sri lankan journal of cardiology - slcc.lk
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An official publication of the
Sri Lanka College of Cardiology (SLCC)
Sri Lankan Journal
of
Cardiology
Volume 3: Issue 2 June 2020
SLJC Editorial Board
Editor in Chief
Dr Ruvan A. I. Ekanayaka Consultant Cardiologist Norris Clinic/ Nawaloka Hospitals PLC.
Editors
Dr Susitha Amarasinghe Consultant Cardiac Electrophysiologist Teaching Hospital, Karapitiya.
Dr S A E S Mendis Consultant Cardiologist Institute of Cardiology, National Hospital of Sri Lanka.
Dr Naomali Amarasena Consultant Cardiologist Sri Jayawardenapura General Hospital.
Dr Mahendra Munesinghe Consultant Cardiothoracic Surgeon
National Hospital of Sri Lanka.
Dr Dimuthu Weerasuriya Consultant Paediatric Cardiologist
Lady Ridgeway Hospital for Children.
International editors
Dr Zahid Amin
Consultant Paediatric Cardiologist Professor and Section Chief Division of Paediatric Cardiology Children’s Hospital of Georgia Augusta University, Georgia, USA.
Dr Sundeep Mishra
Department of Cardiology, All India Institute of Medical Science New Delhi, India.
Dr Rajesh Rajan Consultant Cardiologist President of the Indian Association of Clinical Cardiologists.
Associate editors
Dr Chamara Rathnayake Consultant Cardiologist Asiri Central Hospital, Colombo
Dr Mahen Boralessa
Senior Registrar Institute of Cardiology, National Hospital of Sri Lanka.
The scope of this journal will be broadly
based in order to realize three
objectives.
First and foremost the objective is to
publish high quality research which deals
with problems which are of universal
relevance but with greater focus on work
targeting locally relevant problems.
Secondly, the journal will be a forum for
cardiologists and other specialists to
share their clinical experiences via case
reports. Most cardiologists have cases
worth reporting for their value in
providing insights into pathophysiology,
guiding selection of therapeutic pathways
and shedding light on problem solving.
The journal will encourage such case
reports.
The third objective is for this publication
to be a fruitful avenue of Continuing
Medical Education (CME). The lack of time
should not be a limiting factor to
assimilate knowledge. The journal will
utilize reviews, tutorials, journal scans
and updates to provide a well-balanced
CME course in Cardiology.
Scope of the journal by
Dr Ruvan A I Ekanayaka
ISSN 2630-7596
P A G E | 1
CONTENTS
June 2020 Volume 3 Issue 2
Page
Reviews
Research
Updates
Management of patients with patent foramen ovale E. Chamara Ratnayake
004 ǀ
Page
Updates
Tutorial
Case Reports
A case series of Left Atrial
Appendage (LAA) Device
closure in Sri Lanka W.G Ranasinghe, R.Shetty, V.E Paul, C.J Ponnamperuma, R.S Paranamana, S. Karunarathne, T.D.P Vithanage, D.D.E Colombage, S. Sajeev, W.F.R.D Sovis, V.P Jayasinghe, H.T.R.P Liyanage
COVID -19 Practice Points and
Updates for Cardiologists G Reshmaal Gomes Cumaranatunge
COVID-19 and Acute Coronary
Syndromes: Implications and
considerations F. Aaysha Cader
052 ǀ
COVID-19 Basics for
Cardiologists From the Editorial desk
Rapid Journal Scan From the Editorial desk
044 ǀ
Atrial Fibrillation Management Rohan Gunawardena 007 ǀ
Malnutrition in Children with Congenital Heart Disease – is it a concern? H.M.S.L Jayasekara, T.G Samarasekara, S.N Perera, Renuka Jayatissa, K.H De Silva
Effect of Anticoagulation on the
Lifestyle in Sri Lankan patients with
Mechanical Valves - Prevalence of
Nonfatal Complications of Anti-
coagulation and the Episodes of
deranged INR among the followed up
patients with Mechanical Prosthetic
Heart Valves Palinda Bandarage, Mahendra Munasinghe
013 ǀ
022 ǀ
018 ǀ
060 ǀ
Acute Anterior ST Elevation
Myocardial Infarction
complicated with Ventricular
tachy-cardia due to Diffuse
Coronary Artery Spasms C.P Wickramarachchi, S Senanayake,
K. Lokuketagoda,J. Herath, N. Amarasena
S. Kottegoda
057 ǀ
036 ǀ
P A G E | 2
CONTENTS Continued…….. June 2020
Volume 3 Issue 2
Case Reports
068 ǀ
Page
082 ǀ
070 ǀ
066 ǀ
075 ǀ
Rotational Atherotomy
(Rotablator) assisted
successful PCI in a Heavily
Calcified and Stenosed Right
Coronary Artery C.P.Wickramarachchi, S.Gambhir, K.Lokuketagoda, J.Herath, N.Amarasena
Inferior STEMI due to acute
occlusion of an anomalous left
circumflex artery arising from
the right coronary cusp and
percutaneous coronary inter-
vention of the anomalous
culprit coronary artery M.D.S Boralessa, S.Withanawasam
079 ǀ
Idiopathic Calcific Constrictive
Pericarditis, successfully
treated with Surgical
Pericardiectomy N.U.A. Dissanayake, G.Galappatthy, A.K Pathirana, R.Y. De Silva, C.I.H. Siriwardane, I.U.K. Marasinghe
Distortion and Fracture of the
proximal portion of a stent in the left
main coronary artery that was
successfully managed with a
conservative approach M.D.S Boralessa, S. Withanawasam
062 ǀ
Left Anterior Descending Artery
(LAD) lesion presenting as acute
Inferior ST Elevation Myocardial
infarction (STEMI). A.P.N De Vas Goonewardane, G.I.D De Silva,
J.H Herath, S.R Kottegoda
Retrieval of a Stalled Rotablator Burr
through a modified Double Guide
Technique. T.Kabir, V.Panoulas, A.P.N De Vas Goonewardane
A case of Peripheral Vascular
Intervention for Chronic Total Occlusion
of the Popliteal Artery D.M. Liyanage, N. Fernando, T. Vaikunthan, L.S. Kularatne, T. Pereira
A 27-year-old Lady with Non-
atherosclerotic Spontaneous Left
Anterior Descending Coronary Artery
Dissection. I.H.D.S Prabath, N. Fernando, T. Pereira
073 ǀ
P A G E | 3
CONTENTS Continued…….. June 2020
Volume 3 Issue 2
Brief Reports
Author Guidelines
084 ǀ
086 ǀ
Submitting to the Journal
Clinical and Echocardiographic
patterns of presentation and Immediate
outcomes of Coarctation of aorta
patients following Transcatheter
intervention in a Tertiary Cardiac
Intervention centre in Sri Lanka
S.A.E.S Mendis
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Sri Lankan Journal of Cardiology Volume 3: Issue 2 - June 2020
Management of patients with patent foramen ovale E Chamara Ratnayake
Asiri Central Hospital Norris Canal Road, Colombo 10, Sri Lanka
Corresponding author: Dr. E Chamara Ratnayake Consultant Cardiologist
E mail: [email protected]
Introduction Patent foramen ovale (PFO) has been known to be
involved in the pathogenesis of multiple medical
conditions. However, they have remained an
enigma with no clear guidance as to how best to
approach them. The most conclusive evidence is in
its pathogenesis towards left sided
thromboembolism, mainly leading to cryptogenic
cerebrovascular accidents. As of 2019, there were
no official position papers on its management
mainly because the majority of evidence were
observational and had disparate or contradictory
guidance. To address this concern, the European
Association of Percutaneous Cardiovascular
Interventions (EAPCI) with the collaboration of
eight scientific societies and experts introduced a
position statement on the management of PFO
published online (ahead of print) in October 2018
on the European Heart Journal. This review article
will summarize its content.
PFO related cryptogenic left circulation thromboembolism : Definition, pathogen-esis and evidence
The Cryptogenic ischaemic left circulation
embolisms are defined as any definite ischaemia
(symptomatic or asymptomatic) occurring in an
arterial bed which lacks a known cause despite
investigation. It is recommended that any patient
who presents with the above be screened for PFO
and if found to be causative be reclassified as PFO
related and not cryptogenic.
The possible pathogenesis of thromboembolism
related to PFO is multifactorial. They are (but not
limited to): paradoxical embolism, thrombus
forming within the PFO, left atrial dysfunction,
and atrial arrhythmias.
Multiple clinical observational and randomized
clinical trials have supported the theory that PFO
are indeed culprits in leading to stroke and closure
leads to decline in stroke recurrence compared to
medical therapy.
General approach to PFO management: Common sense should prevail
PFO is a common condition and may be seen in up
to 25% of the general population. Hence, it may
coexist as an innocent bystander in a patient with
unexplained left sided thromboembolism. It
should be considered innocent until proven guilty.
It is recommended to involve a multidisciplinary
team including interventional cardiologists, stroke
physicians, general physicians and any other
speciality demanded by the patient’s clinical
manifestation.
In all clinical scenarios, the two main axes guiding
assessment and treatment of PFO should be: 1) the
probability that any PFO has a relevant role in the
observed clinical picture; 2) the likelihood that the
observed clinical event will recur.
For patients with the highest probability of both,
closure of the PFO should be advised. For patients
with the lowest probability, medical therapy
should be considered. For patients with
intermediate probabilities, clinical judgement is
required to allow good decision with the best
interest of the patient at heart.
Diagnosing PFO: The tools
Diagnosis of PFO is mainly required for the
guidance of treatment. Multiple techniques have
been advocated but the highest quality evidence
stems from the use of two: Contrast enhanced
transoesophageal echocardiography (c-TOE) and
Contrast enhanced transcranial doppler (c-TCD).
Of the two, c-TOE remains the best way of
visualising the inter-atrial septum and any shunt.
However, a metanalysis has shown that the
accuracy of c-TOE compared to autopsy and
cardiac surgery and catheterisation had a
sensitivity of 89%. The slight inaccuracy has been
attributed to the inability of some patients to
perform an adequate Valsalva manoeuvre.
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Sri Lankan Journal of Cardiology Volume 3: Issue 2 - June 2020
The following features should be assessed during
c-TOE to assist in decision making:
• PFO morphology: size, location, length of the
tunnel
• Spatial relationship and distances between the
PFO and the aortic root, vena cava, valves and
the free walls of the atrium
• Comprehensive evaluation of the atrial
septum, including inspection for atrial septal
aneurysms, movement, and other atrial septal
defects
• Presence/absence of a Eustachian valve
and/or Chiari network
• Thickness of the septum primum and
secundum
• Colour Doppler evaluation of the shunt at rest
and after a Valsalva manoeuvre
The use of c-TCD is mainly limited to assessing the
shunt. A metanalysis of 29 studies however yielded
a sensitivity of 94% and specificity of 92%
compared to c-TOE. The use of contrast-
transthoracic echocardiography (c-TTE) provides a
low diagnostic yield with a sensitivity of 88% and
specificity of 82%.
Unfortunately due to the low quality of evidence,
there still remains a question as to what would be
proposed as the gold standard in diagnosis and
management. Current evidence suggests a precise
diagnosis might need a combination of techniques.
The following algorithm has been proposed:
• c-TCD negative – No need of further
evaluation
• If c-TTE positive → c-TOE
• If c-TCD positive → c-TOE
• If c-TTE negative or equivocal → c-TCD
(And as above)
Apart from imaging studies, identifying atrial
fibrillation (AF) is important because recurrences
of left circulation embolism are, in the majority of
cases, due to left atrial appendage thrombosis
instead of paradoxical embolism. A routine 12-lead
electrocardiogram (ECG) and either inpatient
cardiac telemetry or 24-hour Holter monitoring are
sufficient to diagnose permanent AF and
sufficiently long transient AF episodes.
Risk factors associated with PFO-mediated stroke: How likely is it?
Patient characteristics
• Age <55 years
• Absence of other risk factors or
comorbidities for stroke
Imaging stroke pattern
• Cortical infarcts
(Neither the localization nor type of infarct pattern
in grey or white matter was specific for PFO
embolism in observational studies)
Characteristics of the PFO
• Atrial septal aneurysm
• Moderate-severe shunt
• Large PFO
• Atrial septal hypermobility
• Presence of Eustachian valve and/or Chiari
malformation
• Long PFO tunnel
Best management strategy: Medical or interventional?
Prior to embarking on management strategies, it is
best to possess a unified diagnostic work up for
patient who present with left circulation
thromboembolism (Figure 1).
Figure 1: Algorithm for the diagnostic work-up for left
circulation thromboembolism
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Sri Lankan Journal of Cardiology Volume 3: Issue 2 - June 2020
Upon confirmation, a decision on medical vs
interventional therapy can be made.
Medical therapy
Medical management is recommended in patients
deemed low or uncertain risk for causal link or
recurrence.
The choice has been between antiplatelet agents
versus oral anticoagulants (OAC). Most
metanalysis shows superiority of OACs although
the quality of evidence is considered to be low.
The main complication associated with medical
therapy is bleeding. However, a recent metanalysis
has shown a very low prevalence of 1.1%, mainly
attributed to the young age of patients and short
follow up. Thus, this should be interpreted with
caution. The stroke recurrence rate with medical
therapy in most trials ranged between 3-5%
annually.
Percutaneous closure
PFO closure is recommended in patients deemed
to be at high risk for causal link or recurrence and
between the ages of 18-65 years. Percutaneous
closure is currently the method of choice. There is
no evidence to support surgical closure as first line
treatment unless it is done on an incidentally found
PFO during another valvular surgery.
Primary success rates for percutaneous closures
approach 100% and complete closure is seen in
approximately 95% of patients at one year. The
recommended devices thus far are AMPLATZER
and PFO Occluder, as they have relative less rates
of residual shunt compared to other devices.
The stroke recurrence rate following percutaneous
closure is very low, with most trials finding a rate
of less than 2% annually.
The most common complication associated with
percutaneous closure is atrial fibrillation, most
often occurring with the first 45 days. Procedure
related complications occur rarely, with device
thrombosis and device embolism being the most
common. The risk of long term mortality is less
than 1 in 1000.
Dual antiplatelet therapy is recommended for 3-6
months post procedure and a single antiplatelet is
recommended for up to 5 years.
Empirically, antibiotic prophylaxis against
endocarditis before an invasive procedure or
intervention should also be considered routinely in
all cases within the first six months after the
implantation and, probably, beyond six months in
patients with a residual shunt.
Conclusion
The best practice for the management of patients
with apparent cryptogenic left circulation
thromboembolism attributed to PFOs remain
controversial. The current guideline and position
statement seeks to shed some clarity in a field that
lacks quality data and large scale clinical trials. The
most important aspect as with any other
cardiovascular disease is risk assessment followed
by appropriate investigations and treatment. The
position statement also acknowledges the scarcity
of data and strongly recommends research
priorities with larger scale RCTs which would
indeed help in better understanding and thus
treatment of a miniscule hole in the heart with the
potential to cause catastrophic consequences.
References 1. PRISTIPINO, C., SIEVERT, H., D'ASCENZO, F., LOUIS
MAS, J., MEIER, B., SCACCIATELLA, P., HILDICK-SMITH, D., GAITA, F., TONI, D., KYRLE, P., THOMSON, J., DERUMEAUX, G., ONORATO, E., SIBBING, D., GERMONPRE, P., BERTI, S., CHESSA, M., BEDOGNI, F., DUDEK, D., HORNUNG, M., ZAMORANO, J., EVIDENCE SYNTHESIS, T., EAPCI SCIENTIFIC, D., INITIATIVES, C. & INTERNATIONAL, E. 2019. European position paper on the management of patients with patent foramen ovale. General approach and left circulation thromboembolism. Eur Heart J, 40, 3182-3195.
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Atrial Fibrillation Management Rohan Gunawardena
Cardiology unit, National Hospital, Sri Lanka
Corresponding author: Dr. Rohan Gunawardena, Consultant Cardiac
Electrophysiologist
E mail: [email protected]
Introduction Atrial fibrillation (AF) remains the most common
cardiac rhythm disorder in the world. It’s
prevalence in the western population is 1 - 2%
rising with increasing age to 9% after 80 years (1).
The prevalence in Sri Lanka has not been studied
but would be expected to be similar to western
rates and perhaps higher considering that we still
have a considerable population with rheumatic
mitral valve disease. The impact of AF is
underestimated, and new evidence suggests that
death rates are doubled in patients with AF and
while the stroke risk is increased, strokes
associated with AF are more severe. It is believed
that up to 1 in 5 of all strokes are due to AF, even
if AF is not documented at the time. Palpitations,
reduced exercise capacity and vascular dementia
associated with AF, significantly impair quality of
life. Left ventricular function is generally impaired
due to irregular, fast ventricular rates compounded
by reduced LV filling due to loss of atrial systole.
The economic impact on health services and
families caring for patients’ is generally under-
estimated (2).
Classification of AF (3)
The new classification is designed to distinguish
AF according to the clinical status of the patient.
This is useful for the practicing physician as it
allows decisions to be made about the
investigations and management strategies for
individual patients.
First diagnosed AF – this is a patient presenting
for the first time to the physician with AF,
irrespective of whether there had been previous
undiagnosed symptoms and symptom severity. It
is at this point that certain investigations need to
be done, patient is categorized into either
paroxysmal, persistent or long-standing persistent
AF and a strategy be made for long term
management.
Paroxysmal AF – AF is self-terminating, usually
within 48 hours but can last for up to 7 days.
Beyond 48 hrs, the chance of self-termination is
low
low and anticoagulation and cardioversion need to
be considered. Note that if the patient is in AF at
first presentation, it may not be immediately clear
as to whether it is paroxysmal or persistent.
Persistent AF – AF lasting longer than 7 days or
needs medical or electrical cardioversion.
Long standing persistent AF– AF has lasted for
more than one year and a decision has to be made
whether to attempt rhythm control.
Permanent AF – In this case a decision has been
made by the physician and patient to accept AF
and not to attempt rhythm control. If at any time in
the course of treatment a decision is made to
attempt cardioversion then the category changes to
long standing persistent.
Initial assessment
A detailed history, examination and blood pressure
measurement needs to be taken to categorize the
type of AF, severity of symptoms and to elicit
possible risk factors and complications (table 1)
and assess risk of stroke. The EHRA (European
Heart Rhythm Association) score (table 2) is
useful for assessing symptoms. The symptoms
considered in this score are those that would be
alleviated by either rhythm or rate control. The
assessment of stroke risk is also important at this
time.
Is there a precipitating factor such as
exercise, emotion or alcohol
Are symptoms during episodes moderate
or severe (see table 2)
How frequent are symptoms and how long
do they last
Is there a history of coronary artery
disease, rheumatic valvular disease,
hypertension, diabetes, peripheral or
cerebral vascular disease, stroke or TIA or
asthma or COAD
Is there a family history of AF
Table 1 – Assessment of precipitating factors
and complications
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Sri Lankan Journal of Cardiology Volume 3: Issue 2 - June 2020
EHRS
Class
Symptoms
I No symptoms
II Mild symptoms – normal daily
activity not affected
III Severe symptoms – daily activities
affected
IV Disabling symptoms – normal daily
activities discontinued
Table 2 - EHRA score of AF related symptoms
Anti-thrombotic therapy
It is worthwhile spending some time to discuss the
assessment of stroke risk as this is a contentious
and somewhat confusing issue. In all patients with
mitral valvular heart disease anticoagulation with
an oral anti-coagulant (OAC) is recommended in
the presence of mitral stenosis or clinically
significant mitral regurgitation. In patients with
non-valvular AF various studies have been done to
assess risk factors and the effectiveness and risks
of OAC with a vitamin K antagonist (VKA) versus
aspirin and clopidogrel. Perhaps the most useful for
practicing physicians is the CHA2DS2VASc
score(4) (table 3). If the score is ≥ 2, then OAC is
recommended. If the score is 1, aspirin 100mg will
suffice though OAC is preferred. Those with a
score of 0 do not need OAC or aspirin.
Risk factor Score
Congestive heart failure/LV dysfunction 1
Hypertension 1
Age ≥ 75 2
Age ≥ 65 1
Diabetes mellitus 1
Stroke/TIA/Thromboembolism 2
Vascular disease 1
Sex - female 1
Table 3 – CHA2DS2VASc Score
It is now established that OAC is superior to
antiplatelet therapy, either aspirin alone or aspirin
plus clopidogrel with no difference in bleeding
events. The novel oral anticoagulants (NOVACs),
the direct thrombin inhibitors, Dabigatran,
Rivaroxaban and Apixaban have been approved by
the FDA. They all have similar efficacy as
Warfarin and a better bleeding profile. The
advantage of this group of drugs is that there is no
need for monitoring such as PT/INR though
reversal is more difficult than warfarin.
They can be used as first line therapy or in patients
who have fluctuating INR’s or intolerant of
warfarin. The only indication for combined
therapy with aspirin/clopidogrel is in patients with
a CHA2DS2VASc score ≥ 2 but who may be
considered as a high risk for bleeding. It is also
important to realize that the stroke risk is same for
paroxysmal, persistent and permanent AF. The
ideal international normalized ratio (INR) is
considered to be 2 – 3. INRs below 2 have been
shown to increase the stroke risk by twofold and
intracranial bleeding increases with INRs > 3.5.
Another area of concern is the use of OACs in the
elderly. This is driven by fear of intracranial
haemorrhage due to falls and other co-morbidities.
A useful tool is the ‘HAS BLED’ scoring system
(table 4) to assess risk of bleeding. A score of ≥ 3
indicates a high risk (5).
Letter Clinical characteristic Score
H hypertension 1
A Abnormal renal or liver
function (1 point each)
1 or 2
S Stroke 1
B Bleeding 1
L Labile INRs 1
E Elderly (age>65) 1
D Drugs or Alcohol (1 point
each)
1 or 2
Table 4 - HAS-BLED Score for assessing risk of
Bleeding
Initial investigations
The 12 lead ECG will show the ventricular rate
during AF and indicate the state of AV conduction.
A very slow ventricular rate in the absence of rate
limiting drugs suggests AV node dysfunction.
Evidence of ischemia and ventricular pre-
excitation should be noted. An echocardiogram is
useful to identify mitral valve disease, atrial
dilatation, LV hypertrophy, LV dysfunction and
evidence of cardiomyopathy. An FBC, TSH and
FBS would also be reasonable tests at this time.
Acute management
The decision to treat acute AF will depend on
patient’s symptoms and ventricular rate. It is
preferable for the ventricular rate to be between 80
– 100 bpm. However, if the patient is in EHRA 1
or 2 and has no cardiac dysfunction, a ventricular
rate above 100 is temporarily acceptable.
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In situations where AF is secondary (Surgery,
Respiratory tract infection) and expected to
resolve spontaneously, rate control with an oral
beta-blocker or non-hydro pyridine calcium
channel blocker is adequate. In patients who are
very symptomatic IV verapamil can be used. IV
metoprolol is also very useful but not freely
available in Sri Lanka.
In patients with depressed LV function or
haemodynamic instability, achieving sinus rhythm
is desirable. This may also be the case in patients
presenting <48 hours after onset of AF. IV
flecainide or propafenone have the most success
(62-94% and 41-91% respectively) in
pharmacologically converting AF to Sinus
Rhythm. Neither is available in Sri Lanka at
present which leaves Amiodarone as the only
alternative. Amiodarone is the preferred choice for
patients with IHD or impaired LV function.
Though efficacy rates of up to 90% have been
reported conversion is delayed compared to
flecainide or propafenone. Amiodarone should
always be given through a central venous line and
though recommended to be given over one hour,
practically it is more effective giving the bolus (3-
5mg/Kg) over a few minutes followed up by an
infusion of 50mg/hr. To maintain SR,
simultaneous oral amiodarone should be started at
100-200mg tds. As amiodarone can cause
hypotension, heart block and intraventricular
conduction defects this regime should only be
undertaken where monitoring facilities are
available.
In patients with AF and a slow ventricular rate the
possibility of a concomitant AV node dysfunction
must be suspected. Atropine may work transiently,
but in most cases temporary pacemaker insertion
and DC cardioversion is needed. In some patients
AF is part of Sick Sinus Syndrome and successful
cardioversion may be followed by sinus
bradycardia or sinus arrest.
In patients who are very unstable and need rapid
control of a very fast heart rate or conversion to
sinus rhythm due to co-morbidity (IHD, Mitral
Stenosis), Direct Current Cardioversion (DCCV)
is the treatment of choice. Biphasic external
defibrillators are preferred because they are more
efficient at successfully cardioverting AF and do
so at a lower energy setting. Even with biphasic
energy, efficiency is improved if higher energy
levels (150J) are used. In practice minimum
starting energy should be 100J (200J monophasic)
and going up to 200J (360J monophasic).
If initial DCC has failed, loading the patient with 3-
5mg/Kg of amiodarone IV will improve the
efficacy. However, this increases the risk of severe
bradycardia or even cardiac arrest and therefore
resuscitation equipment must be available.
Thrombo-embolism is the main risk following
cardioversion. Therefore, anticoagulation is
mandatory before cardioversion of AF lasting for
>48 hour or of unknown duration. These patients
should be anticoagulated with warfarin (INR 2-3)
for at least 3 weeks. If cardioversion is desired
before 3 weeks at the target INR, then trans-
oesophageal echocardiography (TOE) must be
done to exclude LA thrombus. In this case
unfractionated heparin (UFH) or LMWH may be
administered before DCC and warfarin started. in
patients who have AF, documented to be <48 hours
or those needing urgent cardioversion due to
haemodynamic instability or other reasons, DCC
can be done giving UFH or LMWH before
cardioversion. Warfarin should be initiated
immediately and heparin continued until target INR
levels are achieved. In all cases warfarin should be
continued for at least 4 weeks after cardioversion
due to the risk of thrombo-embolism because of
post-cardioversion left atrial dysfunction. Patients
in the category of increased thrombo-embolic risk
must continue OAC or NOVACs lifelong.
Post-operative AF
AF commonly occurs after cardiac surgery peaking
between day 2 and 4. The incidence is 30% for
CABG, 40% after valve surgery and 50% for
combined valve surgery and CABG. Pre-operative
beta blocker or amiodarone, started at least 1 week
before surgery significantly reduced the incidence
of post surgical AF (6,7,8). In patients who develop
AF, rate control is adequate if haemodynamically
stable but cardioversion is needed if unstable.
Anticoagulation with a VKA should be initiated in
all patients with AF > 48 hrs, and continued for 4
weeks after converting to sinus rhythm.
Rhythm or rate control?
The debate of rhythm versus rate control continues.
None of the early randomized studies (AFFIRM,
RACE, AF-CHF) showed morbidity, mortality, or
quality of life benefit of rhythm control over rate
control. However, a more recent study
(ATHENA)(9) has shown reduced hospitalization,
cardiovascular mortality and stroke, suggesting
benefit of maintaining sinus rhythm.
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The assessment of quality of life in the early
studies is criticized as the instruments used (SF 36
for instance) were tools to measure general quality
of life rather than AF symptoms. Quality of life is
significantly impaired by AF symptoms and
reduced exercise capacity and more recent data
show marked improvement in quality of life after
achieving SR. A reasonable strategy would be to
attempt rhythm control in patients still
symptomatic after rate control (class I level B), in
young symptomatic patients as a primary strategy,
in patients with AF due to secondary triggers
which have been corrected (Class IIa level C) and
those with heart failure (class IIa level B). In
elderly patients with an EHRA score of 1, rate
control would be a reasonable option.
Long term management and follow up
Once a patient has been placed in a clinical
category a management strategy needs to be
planned.
Paroxysmal AF: If the episodes are far apart, short
lasting and minimally symptomatic, the patient
may opt for no treatment. Patients with more
severe symptoms or frequent episodes need either
rate or rhythm control. Rate control must always
be initiated together with rhythm control for any
breakthrough episodes, unless it has been shown
that rate is normal during AF. Anticoagulation
must be initiated according to CHA2DS2VASc
score.
Persistent AF: Even if spontaneous conversion to
SR occurs or cardioversion is successful, a
decision has to be made whether long term strategy
is rate or rhythm control. In these patients there is
more impetus to attempt rhythm control.
Permanent AF: If a decision has been made to
allow AF to be the permanent rhythm, then
appropriate rate control and anticoagulation
should be initiated. At any time during follow up a
decision may be made to convert from rhythm
control to rate control or vice-versa. This is also
true about initiating or stopping anticoagulation.
Rate control
Earlier studies recommended strict rate control
aiming to keep the resting heart rate at 60-80 bpm
with an increase to 90-115 bpm with moderate
exercise. However recent studies have shown that
more lenient control, (resting heart rate <110 bpm)
achieves similar symptom control, adverse effects
and quality of life while reducing the need for
hospital visits (10).
Drugs commonly used are beta blockers, non-
dihydropyridine calcium channel blockers and
digoxin. Beta blockers are particularly useful in
patients with high sympathetic tone and those with
ischaemia. Verapamil and diltiazem are equally
effective but should be avoided in patients with
systolic dysfunction. Digoxin is effective for rate
control at rest but not exertion but can be combined
with a beta blocker or calcium channel blocker.
Amiodarone is not the first line therapy for rate
control but may be needed in addition to a beta
blocker or calcium channel blocker in difficult to
control patients. Dronedarone, which is still not
available in Sri Lanka should not be used in
permanent AF for rate control (11).
Rhythm control
Beta blockers and calcium channel blockers are
not effective for rhythm control. Studies have
shown that amiodarone, propafenone, flecainide
and sotalol are all effective with amiodarone being
the most efficient. The number of patients needed
to treat is 3 with amiodarone, 4 with flecainide, 5
with propafenone, and 8 with sotalol(12).
Amiodarone and propafenone are the least pro-
arrhythmic. Amiodarone is the only drug freely
available in Sri Lanka at present. Dronedarone,
when available may become a preferred option as
though it is not as effective as amiodarone it has a
markedly better side effect profile(11).
It is now well established that the origin of non-
valvular AF is rapidly firing foci in the pulmonary
veins (PVs). Isolation of the PVs form the left
atrium by strategically placed lesions using
radiofrequency ablation (RFA) or Cryotherapy can
be an effective non-pharmacological treatment to
achieve rhythm control. This invasive procedure
should be considered in patients who remain
symptomatic in spite of optimal medical treatment.
The procedure is complex and not without
complications, some which are serious. Success is
greater in patients in the early stages of PAF,
without LA dilatation, significant mitral valve
disease or LVH. The clinical benefits include
abolishing of AF, reducing AF burden and need for
anti-arrhythmic drugs and significantly improving
symptoms and quality of life, but more than one
procedure may be needed for satisfactory
outcome(13). The procedure is at present not freely
available in Sri Lanka due to limited access to
necessary equipment and demand for the treatment
of other arrythmias in the few Electrophysiology
centers in the country.
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Pacing and AV node ablation
Permanent pacing may be needed in patients with
very slow ventricular rates during AF or those who
have those with sick sinus syndrome and
alternating AF and bradycardia. Those patients
with severe symptoms and where rate or rhythm
control cannot be achieved, and who are not
suitable or have unsuccessful RF procedures will
also benefit from pacing. In these situations, once
the pacemaker is implanted an AV node ablation
is done creating AV dissociation. This generally
provides significant symptomatic relief but is done
as a last resort procedure as it is irreversible.
Surgical procedures
The surgical maze, a cut and sew procedure in the
LA is very successful in terminating and
maintaining sinus rhythm but is too invasive with
a significant mortality risk. It cannot be
recommended as a standalone procedure though as
part of other cardiac surgery (MV replacement
etc.) it could be considered though significant
complications still occur. A hybrid procedure
using RF energy to create a maze is a much safer
and viable option, especially as an adjuvant to MV
surgery (14).
Adjuvant therapy
ACE inhibitors and ARBs
There is some evidence that ACEIs and ARBs
reduce the incidence of AF in patients with LV
dysfunction and LVH though the evidence is not
robust. It would be logical to use either in a setting
of hypertension or LV dysfunction.
Statins
There is some evidence that statins may prevent
onset of AF after ischaemic events or after cardiac
surgery. The evidence is slim to support statins in
the secondary prevention of AF but given the
demographics of hyperlipidaemia in our region it
is likely that many patients will need statins and
may benefit from whatever effect it will have on
AF.
Follow up
Once initial management has been done it is
important to plan the follow up. The following are
important considerations for follow up which may
change the management strategy.
• Need for anticoagulation – the need for
initiating anticoagulation if risk profile has
changed (new diabetes or hypertension or
recent TIA). Alternatively, the need for
anticoagulation may have passed (post
cardioversion) or patient may need
modification of anticoagulation for other
purposes (surgery).
• Symptoms – Has the patients symptoms
improved, in which case medications may be
reduced. Is there adequate rhythm or rate
control. Does the patient have symptoms
suggesting pro-arrhythmia or side effects of
drugs?
• Change in classification – has a paroxysmal
AF changed to persistent AF or to permanent.
In this case it may be necessary to change
medication or take a decision about
cardioversion.
Summary In conclusion, a stepwise approach to the
management of AF is needed to provide the best
outcome for the patient. Treatment needs to be
tailored for the individual and needs to be reviewed
regularly as patient’s AF and anticoagulation status
can change.
References 1. Stewart S, Hart CL, Hole DJ, McMurray JJ. Population
prevalence, incidence, and predictors of atrial fibrillation in the Renfrew/Paisley study. Heart 2001;86:516-521
2. Kirchhof P, Auricchio A, Bax J, et al. Outcome parameters for trials in atrial fibrillation: executive summary. Recommendations from a consensus conference organized by the German Atrial Fibrillation Competence NETwork (AFNET) and the European Heart Rhythm Association (EHRA). European Heart Journal 2007;28:2803–2817.
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3. Camm AJ, Kirchhof P, Lip GY et al. the Task Force for the Management of Atrial Fibrillation of the European Society of Cardiology Guidelines for the management of atrial fibrillation. European Heart Journal 2010; 31(19): 2369-2429
4. Brian F. Gage, Carl van Walraven, Lesly Pearce, et al. Selecting Patients with Atrial Fibrillation for Anticoagulation. Circulation. 2004;110:2287-2292.
5. Pisters R, Lane DA, Nieuwlaat R, de Vos CB, Crijns HJ, Lip GY. A novel user friendly score (HAS-BLED) to assess one-year risk of major bleeding in atrial fibrillation patients: The Euorpean Heart Survey. Chest 2010; March 18 [Epub ahead of print].
6. Crystal E, Garfinkle MS, Connolly SS, Ginger TT, Sleik K, Yusuf SS. Interventions for preventing post-operative atrial fibrillation in patients undergoing heart surgery. Cochrane Database Syst Rev 2004;4:CD003611.
7. Burgess DC, Kilborn MJ, Keech AC. Interventions for prevention of postoperative atrial fibrillation and its complications after cardiac surgery: a meta-analysis. European Heart Journal 2006;27:2846–2857.
8. Bagshaw SM, Galbraith PD, Mitchell LB, Sauve R, Exner DV, Ghali WA. Prophylactic amiodarone for prevention of atrial fibrillation after cardiac surgery: a meta-analysis. Annals of Thoracic Surgery 2006;82:1927–1937.
9. Stefan H. Hohnloser, M.D., Harry J.G.M. Crijns, M.D., Martin van Eickels, M.D., et al. for the ATHENA Investigators. Effect of Dronedarone on Cardiovascular Events in Atrial Fibrillation. New England Journal of Medicine 2009; 360:668-678.
10. Van Gelder IC, Groenveld HF, Crijns HJ et al. Lenient versus strict rate control in patients with atrial fibrillation. New England Journal of Medicine 2010;362:1363–1373.
11. Singh BN, Connolly SJ, Crijns HJ, et al. Dronedarone for maintenance of sinus rhythm in atrial fibrillation or flutter. New England Journal of Medicine 2007;357:987–999.
12. Lafuente-Lafuente C, Mouly S, Longas-Tejero MA, Bergmann JF. Antiarrhythmics for maintaining sinus rhythm after cardioversion of atrial fibrillation. Cochrane Database Syst Rev 2007;4:CD005049.
13. Rohan Gunawardena, Stephen S Furniss, Ewan Shepherd, Giuseppe Santarpia, Stephen W Lord, John P Bourke. Outcomes Following Catheter Ablation of Atrial Fibrillation in the UK – A Single-centre Cohort Analysis British Journal of Cardiology 2010;17:271–276.
14. Melby SJ, Zierer A, Bailey MS, et al. A new era in the surgical treatment of atrial fibrillation: the impact of ablation technology and lesion set on procedural efficacy. Annals of Surgery 2006; 244:583-592.
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But the children with complex acyanotic heart
diseases are more prone to develop wasting, may be
due to pulmonary hypertension (5). Children with
complex cardiac defects complicated with cyanosis
as well as pulmonary hypertension are at the
greatest risk of a combination of both stunting and
wasting (6).
Children with pulmonary hypertension with
cyanosis may have very limited nutrient intakes
compared to pulmonary hypertension or cyanosis
alone (9). In addition, children with complex lesions
need palliative surgery, or a staged rather than
single repair, may be at higher risk of poor growth,
which require a close monitoring. It is therefore
important to correct nutritional deficits prior to
surgery to minimize post-surgical risk of
complications. Fatigue on feeding leading to low
total nutrient intake, early satiety, anorexia,
vomiting, frequent infections and frequent use of
antibiotics affecting gut flora are the other
additional factors involving in malnutrition.
Apart from above mentioned factors, raised energy
expenditure also contributes to poor growth (10).
Therefore nutrition intervention is mandatory
preoperatively to enhance immune response and
functional reserve.
Ultimately it will reduce the length of hospital stay
and thereby Intensive Care Unit (ICU) cost.
Introduction
The Congenital Heart Disease (CHD) is the
commonest congenital anomaly occurring
approximately 8 in every 1000 live births
worldwide (1). Though there are several lesions in
the heart, eight lesions make up 80% of cases, the
most common of which are Ventricular Septal
Defect (VSD), Patent Ductus Arteriosus (PDA),
Atrial Septal Defect (ASD) and Tetralogy of Fallot
(TOF) (1). Though the new advances in medical and
surgical management have resulted in good clinical
outcomes, growth failure and nutritional
deficiencies are common among children with
CHD which have adverse clinical outcomes as
recurrent pre-operative infection rates, increased
post-operative infection rates and hospital stay (2).
Nutritional impairment and hence poor growth is
common among children with CHD. Children with
CHD experience growth failure during the first few
months of life even though most of them had
normal birth weights (3). The prevalence of
moderate malnutrition (defined as weight for age
between -2SD to -3SD) among infants with CHD is
between 21 and 29% (4).
When we consider the pathophysiology of CHD,
children with cyanotic lesions appear to be having
the greatest risk of stunting, may be due to chronic
suboptimal tissue oxygenation reducing the linear
growth (5).
Malnutrition in Children with Congenital Heart
Disease – is it a concern? HMSL Jayasekara1, TG Samarasekara1, SN Perera1, Renuka
Jayatissa2, KH De Silva2
1. Lady Ridgeway Hospital for Children Sri Lanka
2. Department of Nutrition, Medical Research Institute, Sri Lanka
Corresponding Author: Dr. G. Samarasekara
Email: [email protected]
The incidence of congenital heart disease (CHD) is approximately 8 in every 1000 live births worldwide. Malnutrition and growth
retardation are associated with complex CHD in infancy and childhood. Objective of this study was to determine the prevalence of
malnutrition among children born with congenital heart disease attending a tertiary care cardiology unit.
All CHD children admitted to the cardiology unit at Lady Ridgeway hospital during December 2018 were included. Type of the
cardiac lesion (cyanotic/acyanotic), birth-weight were obtained from the patient’s records. Weight and length/ height were measured,
and WHO standards were used to assess nutritional status.
A total of 39 children were recruited; 25 infants, 9 children aged 1-5 years and 5 children >5 years. Mean age was 20.6 (27.1) months,
two third were females and 64% were acyonatic. Commonest CHD was VSD. Among them, prevalence of severe wasting, severe
stunting and low birth weight (LBW) were 25.6, 30.1 and 25.6 percent respectively. Wasting was significantly higher (p<0.05) in
children with acyanotic heart disease (65.7%) compared to children with cyanotic heart disease (30.4%).
Half of children with CHD had acute malnutrition. Focus on nutrition therapy is important routinely to improve the outcome of CHD
children.
Keywords: Congenital heart disease, malnutrition, stunting, wasting
.
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Sri Lankan Journal of Cardiology Volume 3: Issue 2 – June 2020
The final outcome of nutritional optimization is to
reduce morbidity and mortality.
In Sri Lanka, malnutrition and failure to thrive is
observed in infants and children with CHDs at
clinical settings. But published data is scarce.
Hence this study was conducted to assess the
prevalence and associated factors of malnutrition in
children with CHDs.
Methodology This is a descriptive cross-sectional hospital based
study. Study population was children aged 0-8 years
admitted to the cardiology unit of Lady Ridgeway
Hospital for children (LRH), which is the largest
children’s hospital in Sri Lanka. The study was
conducted in December 2018.
All the children with CHD who were admitted
during the study period was included in the study.
After obtaining the consent from the mother or
caretaker, information was gathered on age, sex and
birth weight from the Child Health Development
Records (CHDR).
Type of the cardiac lesion, cyanotic or acyanotic
and stage was obtained from the patient’s record.
Weight and height or length was measured using
stadiometer and electronic weighing scale by a
trained measurer adopting WHO protocol.
Anthro and Anthro-plus software was used to
analyze the anthropometric data (WHO 2005,
2009). Severe wasting and wasting were defined as
weight-for-height < -3SD and < -2SD for children
below 5 years and BMI-for-age < -3SD and < -2SD
for children above 5 years respectively. Severe
stunting and stunting were defined as height-for-
age < -3SD and < -2SD respectively. Data was
analyzed using SPSS software package version 24.
Results
A total of 39 children with CHD was recruited.
Table 1 shows majority of children were below five
years of age (82%), females (69.2%) and 64.1% had
acyanotic heart diseases.
Table 2 shows the prevalence of malnutrition of the
study population namely stunting and wasting. The
prevalence of severe stunting is 25.6% in the study
population. About 30% of children were severely
wasted while half (51.6%) of children were wasted.
Characteristics No (%)
Age categories in months
< 12 25 (64.1)
12 - 59 9 (17.9)
≥ 60 5 (17.9)
Mean age ± SD 20.6 ± 27.1
Range 1 – 96 months
Sex
Male 12 (30.8)
Female 27 (69.2)
Stage of CHD
Cyanotic 14 (35.9)
Acyanotic 25 (64.1)
Type of CHD
VSD 11 (28.2)
TOF 9 (23.1)
PDA 6 (15.4)
IAS 3 (7.7)
Transposition of great arteries 3 (7.7)
Many lesions 5 (12.8)
Birth weight in kg
< 2.5 10 (25.6)
≥ 2.5 29 (74.4)
Mean birthweight ± SD 2.8 ± 0.5
Range 1.8 – 3.7
Table 1: Basic characteristics of study
population (n=39)
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Sri Lankan Journal of Cardiology Volume 3: Issue 2 – June 2020
Table 2: Prevalence (%) of malnutrition of the study population
Anthropometric indicators Severe
< -3SD
Moderate and severe
< -2SD
Other
≥ 2SD
Stunting (Chronic malnutrition) 25.6 46.2 53.8
Wasting (Acute malnutrition) 30.1 51.6 48.4
Table 3: Prevalence (%) of malnutrition of the study population in relation to basic characteristics
Basic
characteristics
Stunting
(height-for-age <-2SD)
Wasting
(weight-for-height <-2SD)
Yes No Yes No
Age in months
< 12 48.0 52.0 60.0 40.0
12 - 59 33.3 66.7 37.5 62.5
≥ 60 60.6 40.0 20.0 80.0
Sex
Male 58.3 40.7 62.5 37.5
Female 40.7 59.3 47.9 52.1
Stage of CHD
Cyanotic 42.9 57.1 30.4 69.6
Acyanotic 48.0 52.0 *65.7 34.3
Type of CHD
VSD 45.5 54.5 *86.4 13.6
TOF 44.4 55.6 30.9 69.1
PDA 33.3 66.7 55.0 45.0
Others 53.8 46.2 35.4 64.6
Birth weight in kg
< 2.5 60.0 40.0 66.9 33.1
≥ 2.5 41.4 58.6 49.9 50.1
Total 46.2 53.8 51.6 48.4 *(P<0.05)
48% of children under 1 year were stunted while 60
% of children were wasted as shown in Table 3. One
third of children between 12 to 59 months were
stunted and wasted while 60% of children more
than 5 years were stunted.
Male or female gender did not show any significant
association with wasting and stunting.
Similar prevalence of stunting was observed among
children with acyanotic heart diseases (48%)
compared to children with cyanotic heart diseases
(42.9%).
Wasting was significantly higher (p<0.05) in
children with acyanotic heart disease (65.7%)
compared to children with cyanotic heart disease
(30.4%).
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Sri Lankan Journal of Cardiology Volume 3: Issue 2 – June 2020
The children with LBW had higher prevalence of
stunting (60% Vs 41.4%) compared to children
born with a birth weight above 2.5 kg though it was
not significant. Wasting was higher among children
with LBW compared to children with normal birth
weight (66.9 vs. 49.9%).
Discussion Malnutrition is more common among children with
congenital heart disease due to difficulties in
establishing total energy requirement with
restricted fluid intake during the neonatal period.
Apart from the increased energy requirements with
increased cardiac workload, recurrent respiratory
tract infections, and difficulties in supplying energy
requirements with complementary feeding and
frequent recurrent hospital admissions are other
concerns (14).
Our study has shown that the severe malnutrition
among children with CHD is 30.1%, which is much
higher when compared with available national data
which is 3.0% (12). The children included in our
study were admitted to the ward awaiting cardiac
surgery. Most of them had been on the waiting list
for several months due to lack of facilities which
may be the main reason for inadequate calorie
intake with multiple co factors such as maternal
anxiety, lack of frequent visits due to far away home
towns, economic problems, lack of facilities to
prepare meals, lack of play areas and minimum sun
exposure. Apart from inadequate caloric intake,
malabsorption, and increased energy requirements
caused by increased metabolism may also
contribute to malnutrition. However, inadequate
caloric intake appears to be the most important
cause of growth failure in CHD. Optimizing
nutritional status improves surgical outcome and
contributes to reduced morbidity and mortality.
Significantly higher prevalence (65.7%) of wasting
among acyanotic heart disease children could be
due to increased physical activity compared to
children with cyanotic heart disease (4). Children
with cyanotic heart disease are prone to develop
more complications leading to limited physical
activity and reduced mobility therefore less energy
requirement with less under nutrition. In contrast
to that, children with acyanotic heart disease are
active with increased energy requirements as well
as with increased susceptibility to infections (13).
The national prevalence of stunting is 17.3%, which
is lower than the stunting prevalence (46.2%) in our
study (12). Childhood stunting can have long term
effects on cognitive development, school
achievements and economic productivity in
adulthood and maternal reproductive outcomes (11).
Ultimately this will lead to reduced productivity in
future in Sri Lanka. But there is no significant
difference of prevalence of stunting among
cyanotic or acyanotic heart disease (p = 0.697).
These facts highlight the importance of early
intervention to prevent malnutrition among children
with congenital heart disease. Early surgical
intervention as well as effective and early
nutritional interventions are important for
prevention and slowing down of development of
malnutrition. As first thousand days are important
for optimum growth and development of every
child, importance of earliest possible interventions
is highlighted with the results.
There is increased morbidity and mortality among
low birth weight infants with congenital heart
disease compared to normal population (3). The
prevalence of low birth weight among live births in
Sri Lanka is 15.7% while prevalence of low birth
weight is higher (25.6%) among study population (12).
Malnutrition in children with CHD leads to a
vicious cycle which will worsen both malnutrition
and complications of CHD which can be corrected
by, with earliest possible, optimum and
individualized interventions.
The results could be different with a larger sample
which needs further research. Disease
categorization could be more precise if presence of
pulmonary hypertension is also included.
Conclusion
Prevalence of acute and chronic malnutrition is
higher among children with CHD with higher
numbers from acyanotic heart disease. Further
research is needed with extensive disease
categorization to identify reasons for malnutrition
and associated factors of malnutrition to improve
the outcome. There is an urgent need to provide
nutrition therapy for these children and advice to the
parents/guardians.
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Sri Lankan Journal of Cardiology Volume 3: Issue 2 – June 2020
References 1. Noonan J Noonan syndrome and related disorders.
Progress Pediatr Cardiol, 2005, 20177-8. 2. Wynn Cameron J, Rosenthal MD, Olson AD
Malnutrition in hospitalized children with congenital heart disease. Arch Pediatr Adolesc Med, 1995, 149: 1098-102.
3. Jacobs EGJ, Leung MP, Karlberg JP Postnatal growth in southern Chinese children with symptomatic congenital heart disease. J Pediatr Endocrinol Metab, 2000, 11195-202.
4. Varan B, Tokel K, Yilmaz G. Malnutrition and growth failure in cyanotic and acyanotic congenital heart disease with and without pulmonary hypertension. Archives of Disease in Childhood, 1999 Jul 1; 81(1): 49-52.
5. Waterlow JC Protein Energy Malnutrition. London: Edward Arnold, 1992: 231-2.
6. Farrell AG, Schamberger MS, Olson IL, Leitch CA Large left-to-right shunts and congestive heart failure increase total energy expenditure in infants with ventricular septal defect. Am J Cardiol, 2001; 871128-31.
7. Barton J, Hindmarsh P, Scrimgeour C. et al. Energy expenditure in congenital heart disease. Arch Dis Child, 1994; 705-9.
8. Ocal B, Unal S, Zorlu P. et al. D Echocardiographic evaluation of cardiac function and left ventricular mass in children with malnutrition. J Paediatr Child Health, 2001, 3714-17.
9. Soliman A, Madkour A, Abdel Galil M et al. Growth parameters and endocrine function in relation to echocardiographic parameters in children with ventricular septal defect without heart failure. J Trop Pediatr, 2001; 47146-52.
10. Thommessen M, Heiberg A, Kase B Feeding problems in children with congenital heart disease: the impact on energy intake and growth outcome. Eur J Clin Nutr, 1992; 46457-64.
11. Kathryn G. Dewey and Khadija Begum, Long-term consequences of stunting in early life. Maternal and Child Nutrition 2011; 7(Suppl. 3): 5-18.
12. Department of Census and Statistics. Demographic and Health Survey 2016. Government of Sri Lanka. Colombo. 2017.
13. Pujitha Wickramasinghe SPL and SN. Prospective study of congenital heart disease in children. Ceylon Medical Journal, 2000; 96-8.
14. M.P. Gamage, K. Sithamparapillai, S.N. Perera, Randula Ranawaka, Renuka Jayatissa, Prevalence of malnutrition in children with Congenital Heart Disease awaiting cardiac interventions at a tertiary care setting in Sri Lanka. Sri Lankan Journal of Cardiology, January 2019; 1(2): 39-43.
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Sri Lankan Journal of Cardiology Volume 3: Issue 2 – June 2020
While the mechanical cardiac prosthetic valves
unlike bioprosthetic valves have the advantage of
outliving the patient with no need of redo surgery,
being on lifelong anticoagulation is essential to
prevent thrombus formation on the valve’s
surface. Although there are novel oral
anticoagulants used for other conditions these are
not currently indicated for the use for
anticoagulation of patients with mechanical valves (2).
Though it is a necessity for the patient to take oral
anticoagulants uninterrupted, the complex
pharmacokinetics and the wide array of
interactions sometimes make it a difficult task to
maintain a stable International normalized ratio
INR (3). While sub-therapeutic anticoagulation
with low INR can lead to thromboembolic
complications, excessive anticoagulation can
cause haemorrhages (4). Both these complications
increase the morbidity and mortality of the
condition. Furthermore very regular checking of
INR with dose adjustments and management of
sub or supra therapeutic levels of the anticoagulant
is a burden the patients with mechanical valves
have to face (5).
Currently, according to international literature the
average prevalence of overall valve related
complications stands at 0.7% to 3.5% per patient
years (1,6). Out of this, thrombosis associated valve
complications were seen at a rate of nearly 1% per
patient year and prevalence of haemorrhagic
complications were approximately 0.5% per
patient year.
Introduction
While the surgical management of valvular heart
disease is increasingly popular globally, it has
become reasonably accessible now in low income
countries as well. With the technological advances
in this respect, the immediate outcome and patient
survival rate over the decades have dramatically
improved, but life-long anti-coagulation therapy
remains mandatory for all mechanical valve
prostheses. Hence it is inevitable that we have to
face the challenges of long-term anticoagulation
that brings its own complications, mainly
haemorrhagic or thrombotic. Although the
anticoagulation therapy carries a high burden on
the patient, detailed studies/research in to the
situation in Sri Lankan patients are scarce. This
study was designed with the intention of
identifying the frequency of complications
associated with mechanical prosthetic valves
among the patients who present for follow up and
are on long-term anticoagulation.
Literature review
Worldwide, the overall outcome of cardiac
valve replacement surgery has improved with the
10 year survival reaching above 60% even among
most high risk patient groups. Nonetheless, the
associated morbidity due to valve related
complications remains significant.
Thromboembolism, haemorrhagic episodes and
prosthetic valve endocarditis are the common
complications associated with the prosthetic
valves and the mandatory anticoagulation therapy (1).
Ab
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Effect of Anticoagulation on the Lifestyle in Sri Lankan
patients with Mechanical Valves - Prevalence of
Nonfatal Complications of Anticoagulation and the
Episodes of deranged INR among the followed up
patients with Mechanical Prosthetic Heart Valves
Palinda Bandarage 1, Mahendra Munasinghe 2
1. Specialist registrar, Cardiothoracic Surgery. Oxford University Hospital.UK
2. Department of Cardiothoracic Surgery, National Hospital of Sri Lanka.
Corresponding Author: Dr. M Munasinghe. Consultant Cardiothoracic Surgeon Email: [email protected]
While mechanical valve prosthesis remains the ideal choice for valve replacement where longevity is concerned, the mandatory anticoagulation
with warfarin leaves such patients at risk of haemorrhagic and thrombotic complications. This effects the patient’s lifestyle and is a burden to
the health services. Although the long-term outcome of oral anticoagulation in valve patients is a common topic in international literature,
studies in Sri Lankan patient population is scarce. This was a retrospective observational study including all the patients who were being
followed up following mechanical valve replacement between January 2010 and December 2014 in a cardiac surgical unit in the National
Hospital of Sri Lanka. A total of 148 patients were followed up. A significant number of patients had hospital admissions with deranged INR
having variable durations of stay. Overall complication rates were less compared with the literature, possibly explained by the fact that
untraceable and deceased patients could not be included in the study. A more robust follow up and incident reporting system would beneficial
to improve the situation.
Keywords: Anti Coagulation, INR, Mechanical valves
.
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Sri Lankan Journal of Cardiology Volume 3: Issue 2 – June 2020
Table 1: Approximate prevalence of mechanical valve related complications (1)
All valve related
complications
Thromboembolic
complications
Haemorrhagic
complications
% per patient year 0.7 – 3.5 Approximately 1.0 < 0.5
Type of valve prosthesis Aortic - 58 Mitral - 80
Gender Male - 68 Female - 80
Employment Employed - 67 Unemployed - 81
Age at surgery < 50 yrs - 62 > 50 yrs - 86
In a study which followed up 440 patients with St
Jude mechanical valve implantation in the mitral
position for 19 years it was found that thrombo-
embolic and haemorrhagic complications were
0.7% and 1% patient-years respectively (7).
The valve type, its position, and co existing
cardiac factors such as the atrial dilatation, atrial
fibrillation increase the risk of major valve
associated complications. Furthermore good
patient compliance with regular assessment of
INR levels and optimizing of the warfarin dose is
essential. On the other hand warfarin being a
drug with many interactions including a number
of food items and drugs, demands optimum
patient compliance to maintain the anti-
coagulation in the desired range (3). Considering
all these intricacies, in the current era, use of
novel oral anticoagulants may benefit Sri
Lankan patients.
A similar study done in the Indian setting showed
that a statistically significant wide variation in
INR among patients with combined aortic and
mitral valve replacements and isolated AVR,
leading to high risk of thromboembolic and
haemorrhagic complications (8).
Methods
This was a retrospective, observational study
in which the study population included all the
patients who underwent mechanical valve
replacement between January 2010 and
December 2014 and were scheduled for long-
term clinic follow up at the National Hospital
Cardiothoracic clinic.
Patients who underwent valve repair and patients
who had bioprosthetic valve replacements were
excluded. Similarly patients who underwent
mechanical valve replacement but opted to get
followed up in their local hospital clinics and
patients who defaulted anticoagulation therapy
were excluded.
Data were collected using an interviewer
administered questionnaire at the clinic visit.
Results
There were 148 patients with mechanical heart
valves that were followed up in the clinic within
the duration planned to be studied accounting for
888 total patient years.
Mean number of admissions for INR correction
per patient year was 0.74 while the mean number
of days per patient year spent inward for INR
correction was 4.44. The exact number of
admissions and number of days spent in ward
were highly variable and varied between 0 to 4
admissions and 0 and 14 days per year
respectively.
There were 24 patients who developed
haemorrhagic episodes, implying a rate of
0.451 haemorrhagic episodes per 10 patient
years. Furthermore 4 patients developed
thromboembolic episodes amounting to 0.045
per patient year. The rate of total neurological
complications per 10 patient years was 0.136.
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Sri Lankan Journal of Cardiology Volume 3: Issue 2 – June 2020
Conclusion
The number of admissions to ward and the time
spent in ward were highly variable while some
patients had a high frequency of admissions and
longer hospital stays.
The rate of both haemorrhagic and thrombotic
complications seen were significant but were
lower, when compared to most of the studies
in similar settings found in the literature.
Discussion
It is notable that the complication rate reported in
the study was low compared to most parallel
studies in the literature (1,3,6). Although strict
regular follow up with timely assessment of INR
is a must in all patients with mechanical
prosthetic valves, a significant proportion of
patients fail to follow this rule due to various
reasons (6). The population recruited for the study
was the total number of patients who voluntarily
presented for regular follow up in the same
hospital they underwent valve replacement.
Although this included the majority of the post-
operative patient population it did not include the
patients who opted to get followed up in the
local hospital haematology clinics for
convenience.
The identification and quantification of the exact
number of defaulted patients were practically
impossible due to this reason. This fact highlights
the need of a robust follow up and reporting
mechanism where defaulters can be approached
by a community health staff officer (9).
The number of admissions was significantly high
in the study population with a wide individual
variation. Although parallel results were not
available in the literature to compare how the
derangements in INR and subsequent hospital
admissions affect the lifestyle and employment
of patients it is the belief of the research team that
measures to stabilize the INR and ensure regular
follow ups will increase the quality of life in these
patients. Furthermore, a drawback in the study is
failure to consider the fatal complications among
followed up cases.
This holds true for any system lacking proper
community follow up such as ours.
Hence the rate of complications will be
misleading as any fatalities among the clinic
patients and complications of any degree among
patients lost to follow up had to be exempted
from the study due to practical reasons.
One key fact that facilitates smooth management
of anticoagulation therapy is the patient’s
knowledge regarding the treatment and the
vigilant identification of early signs of
haemorrhage or thrombosis. As warfarin has a
narrow therapeutic window with a number of
drug to drug and drug to food interactions,
counselling and regular updating is vital (10). This
is definitely an area for improvement in the local
setting.
In conclusion the population of patients
presenting for follow up had minimal
complications compared to the international
average but some had to undergo significant
durations of in ward treatment for correction of
deranged INR. Avoiding mechanical valves by
repairing the valves whenever possible and using
newer generation valves with lesser need of
anticoagulation are prospective options, which
would have a positive impact.
References 1. Misawa Y. Valve ‑ related complications after
mechanical heart valve implantation. Surg Today [Internet]. 2015;1205-9. Available from: http://dx.doi.org/10.1007/s00595-014-1104-0
2. Aimo, A., Giugliano, R. P. & DC. Non – Non–Vitamin K Antagonist Oral an ticoagulants for Mechanical Heart Valves. Circulationaha,. 2018; 138(13):1356-65.
3. Labaf A, Grzymala-lubanski B, Stagmo M, Lövdahl S, Wieloch M, Själander A, et al. Thromboembolis, major bleeding and mortality in patients with mechanical heart valves- a population-based cohort study. Thromb Res [Internet], 2014; 134(2): 354-9. Available from: http://dx.doi.org /10.1016/j.thromres.2014.06.00.
4. Kratz JM, Iii AJC, Stroud MR, Bradley SM, Sade RM,
Crawford FA. Twenty-year experience with the St
Jude Medical mechanical valve prosthesis. 2003
(December).
5. Kandemir O, Tokmakoglu H, Yildiz U, et al. St. Jude
Medical and CarboMedics mechanical heart valves
in the aortic position: Comparison of long-term
results. Texas Hear Inst J, 2006; 33(2): 154-9.
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6. Canicelli A. Anticoagulation for Valvular Heart Disease - American College of Cardiology. Am Coll Cardiol. May 2015.
7. Despins P, Michaud JL, Duveau D. Isolated Mitral Valve Replacement With St Jude Medical Prosthesis. 2001; (Table 1): 1542–5.
8. Ujjwal K Chowdhury, Pranav Sharma, Lakshmi Kumari Sankhyan, et al. Annals of Short Reports Thromboembolic and Bleeding Complications following St Jude’s valve replacement. Rem Publ. 2018; 1(2): 1009.
9. Jaffer A, Bragg LEE. Practical tips for warfarin. 2003; 70(4): 361-71.
10. Kuruvilla M G-TC. Pharmacology NNotes. Proc (Bayl Univ Med Cent). 2001; 75246: 305-6.
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Sri Lankan Journal of Cardiology Volume 3: Issue 2 - June 2020
COVID -19 Practice Points and Updates for
Cardiologists
G Reshmaal Gomes Cumaranatunge 1
1. Consultant Cardiologist, Phoenix, Arizona, USA
Corresponding author: E-mail: [email protected]
Introduction Physicians have been impacted by the 2019 novel
coronavirus, or severe acute respiratory syndrome
coronavirus-2 (SARS-CoV-2) that results in
coronavirus disease-2019 (COVID-19),
irrespective of where they trained or where they
practice currently. We were all bombarded with
treatment options on a daily basis. What was
thought to be Best Practice in February 2020 may
well not be so today.
So how do we navigate through this myriad of
information?
Below are some practice points and updates
compiled from recent recommendations from
American College of Cardiology and local practice
here in Arizona as of June 20th 2020.
How should Acute Myocardial Infarction be managed during COVID-19? (1)
COVID-19 patients are complex: patients may present with acute myocardial infarction (AMI),
myocarditis simulating a STEMI, stress cardiomyopathy, nonischemic cardiomyopathy, coronary spasm, or myocardial injury without a
documented Type I or Type II AMI, requiring careful diagnostic differentiation to maximize therapeutic effectiveness and minimize
unnecessary medical staff exposure risk. Nonetheless, most AMI cases remain COVID
negative and should be managed aiming at
expedient revascularization according to standard
PCI protocols.
Fibrinolysis-based reperfusion strategy may be
appropriate in non-PCI capable hospitals,
especially when timely transfer is not practical, or
when otherwise clinically indicated.
AMI standard-of-care during COVID-19: All
efforts should be made to maintain the current
AMI standard-of-care.
Door-to-balloon times remain important and
should continue to be measured; however,
additional time may be required for careful clinical
differentiation of both COVID status and precise
MI etiology to minimize exposure risk and ensure
the appropriate therapeutic intervention.
AMI management protocols in the context of
pandemic COVID-19 should be developed in
advance, and include ambulance/EMS, the
Emergency room and the cardiac
catheterization laboratory (CCC). Dedicated
COVID-19 CCLs and PPE should be available
in geographies with widespread community
transmission.
• Definite STEMI: Primary PCI within 90
minutes remains the standard-of-care in PCI
capable hospitals regardless of COVID status.
Additional exposure precautions are
mandatory in probable and confirmed
COVID-19 patients, but may be considered
for all cases given asymptomatic presentation
and the potential for false-negative COVID
test results.
• Possible STEMI: For patients who have an
unclear, or equivocal, diagnosis of STEMI due
to atypical symptoms, diffuse ST-segment
elevation or atypical ECG findings, or a
delayed presentation, additional noninvasive
evaluation is recommended.
• Futile prognosis: Not all COVID-19 patients
with ST elevation with/without an acute
coronary occlusion will benefit from any
reperfusion strategy or advanced mechanical
support.
• In COVID-19 confirmed patients with severe
pulmonary decompensation (adult respiratory
distress syndrome) or pneumonia who are
intubated in the ICU and felt to have an
excessively high mortality, consideration for
compassionate medical care may be
appropriate.
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Cardiomyopathy has been described in patients
with severe COVID-19 disease and increasing
evidence suggests that cardiovascular involvement
portends a high mortality. Viral infection with
SARS-CoV-2, the causative agent of COVID-19,
has been proposed to impact cardiac function via
at least three distinct mechanisms.
First, the later phase of COVID-19 disease is
associated with a profound systemic inflammatory
response. The cytokines released during this phase
have the potential to trigger cardiomyocyte
dysfunction and cardiac depression.
This phenomenon has been well described in other
inflammatory conditions such as sepsis, where
TNFα and IL-1β/β directly suppress
cardiomyocyte contractility.
Second, SARS-CoV-2 can directly infect the heart
leading to immune cell recruitment and
myocarditis. To date, there are few data from
patients with COVID-19 to gauge the exact
frequency of myocarditis. However, the heart
expresses the SARS-CoV-2 receptor ACE2 and
MRI-based imaging and ECG findings of
myocardial involvement have been reported(2,3).
In addition, a study of the related virus SARS-
CoV-1, which also uses ACE2 for cell entry,
demonstrated the presence of viral RNA in 35% of
hearts at autopsy. Interestingly, cardiac tissue from
patients with positive viral RNA had an increase in
macrophage infiltration, but not a substantial T-
cell response.
Third, infection with SARS-CoV-2 could impact
the microvasculature via its effects on ACE2. This
could trigger microvascular dysfunction and tissue
ischemia leading to ventricular dysfunction and/or
arrhythmias.
Ongoing investigation and further autopsy studies
will be necessary to determine the proportion of
patients with secondary vs. primary cardiac
involvement. Those with underlying
cardiovascular disease are particularly vulnerable
to the cardiac effects of COVID-19-induced
inflammation.
In severe COVID-19 cases, cardiomyopathy may
result from SARS-CoV-2-induced myocarditis,
profound systemic inflammation, and/or
microvascular dysfunction.
• Non -STEMI capable referral hospitals:
Primary PCI remains the standard of care for
patients transferred rapidly from non-PCI
centers (within 120 minutes of first medical
contact at Referral Hospital).
• For patients in whom rapid reperfusion with
primary PCI is not feasible, a
pharmacoinvasive approach is recommended
with initial fibrinolysis followed by
consideration of transfer to a PCI center.
• The COVID status of the individual patient,
along with the COVID burden at both the
referring and receiving hospital may require
modifications to this standard.
• Cardiogenic shock and/or out-of-hospital
cardiac arrest: Patients with resuscitated out-
of-hospital cardiac arrest (OHCA) and/or
cardiogenic shock will continue to be the
highest risk subgroup of AMI patients.
• These patients will also be the highest risk for
droplet-based spread of COVID-19. Patients
with resuscitated OHCA should be selectively
considered for CCL activation in the presence
of persistent ST-elevation on their
electrocardiogram, and a concomitant wall
motion abnormality on echocardiographic
evaluation.
• Non-ST elevation AMI: (Standard of care to
both COVID positive and negative patients):-
COVID-19 positive or probable patients with
an NSTEMI presentation should be managed
medically and only taken for urgent coronary
angiography and possible PCI in the presence
of high-risk clinical features (Global Registry
of Acute Coronary Events [GRACE] score
>140) or hemodynamic instability.
What are the considerations for cardiomyopathy and heart failure in COVID-19? (2)
Cardiac dysfunction is moderately common among hospitalized patients with COVID-19 and
confers a worse prognosis; focused imaging and other cardiac diagnostics are warranted to guide differential management, but must be balanced against exposure risk; clinical management
remains supportive although experimental
strategies are being evaluated.
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There is currently very little data to guide the
optimal management of patients with COVID-19
disease who develop cardiomyopathy or
mixed/cardiogenic shock.
Cardiac imaging may be useful, but only when
testing is likely to result in differential
management and exposure risk can be adequately
mitigated.
• In patients hospitalized with COVID-19
cardiac biomarkers (troponin and natriuretic
peptide levels) should be checked on
admission and in follow-up approximately
24-48 hours later. Increased troponin and
natriuretic peptide levels have a worse
prognosis.
• Myocarditis or inflammatory cardiac
dysfunction should be considered in patients
with COVID-19 who have elevated cardiac
biomarkers and worsening hemodynamics or
arrhythmias.
• ECG should be employed to screen for
evidence of ST-T wave changes can include
diffuse ST-elevations as seen in
myopericarditis, nonspecific ST changes,
low voltage in the limb leads, and PVCs.
Patients can also present with STEMI in the
setting of COVID-19 and often without
evidence of coronary obstruction, perhaps
secondary to myocarditis or direct cardiac
injury from the virus.
• Maintain a low threshold for point of care
ultrasound (POCUS) in patients with the
above clinical features.
• If evidence of cardiac dysfunction, select
view for transthoracic echocardiography
(TTE) to define LV/RV size and function,
wall motion abnormalities, and/or pericardial
effusion. In most cases, a limited study can
provide the necessary information for
medical decision-making.
• Stable patients with suspected cardiovascular
involvement should continue on guideline-
directed medical therapy for heart failure.
• In patients with refractory shock, consider
pulmonary artery catheters to help guide the
use of inotropes, vasopressors or mechanical
support.
• Endomyocardial biopsy may have a role in
select patients being considered for clinical
trials of anti-inflammatory therapy.
Management of Cardiomyopathy in COVID-19- Medical Supportive Care
The mainstay of managing patients with severe
COVID-19 disease who have cardiac involvement
is supportive care. There is currently no evidence
to direct the management of these patients
differently than any other inflammatory or
"mixed" shock state.
Some general principles include:
• Avoid overaggressive fluid resuscitation
given challenges with oxygenation (target
CVP 6-8 mm Hg). Higher preload (CVPs 12-
15) may also be desirable when significant
RV dysfunction and/or high positive end-
expiratory pressure (PEEP) states are
present. The effective CVP can be calculated
by measured CVP – PEEP.
• Target a MAP of 60-65 mm Hg and
preferentially start with norepinephrine
infusion for hypotension.
• Consider dobutamine in the setting of
worsening hypotension with cardiac
dysfunction.
• Epinephrine and vasopressin should be
considered for refractory hypotension.
• Consideration can be given to using
Angiotensin II for refractory vasoplegia.
Mechanical Support/ECMO
There are several factors that must be considered
prior to placing a patient with COVID-19 on
ECMO support. ECMO is a limited resource and
should be reserved for those with the greatest
chance of recovery. Therefore, ECMO should not
be considered in futility.
• The majority of patients being considered for
ECMO with COVID-19 disease will have
refractory hypoxemia and respiratory acidosis
despite advanced ventilator management.
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In these patients, VV ECMO via internal
jugular vein access is most appropriate.
• However, in patients with significant
cardiomyopathy and cardiogenic shock, a
VA ECMO configuration might be
necessary.
As discussed above, the use of hemodynamic
surrogates and echocardiogram findings can help
direct this decision. To this end, VA ECMO has
been used to successfully support a patient with
COVID-19 who had combined respiratory failure
and cardiomyopathy.
• As the majority of patients with circulatory
failure also have profound hypoxia, the
utility of other cardiac support devices such
as intra-aortic balloon pump, TandemHeart
or Impella is limited.
• The mainstay of managing patients with
severe COVID-19 disease who have cardiac
involvement is supportive care.
• There is currently no evidence to direct the
management of these patients differently
than any other inflammatory or "mixed"
shock state.
• Experimental strategies including antiviral,
anti-inflammatory, convalescent sera are
being considered as part of research
protocols or compassionate use for COVID-
19 infection with or without cardiac
involvement.
What are the key considerations for managing AFib during COVID-19? (3) While there is no evidence of a direct association between COVID-19 and new-onset atrial fibrillation (AFib), serious viral illness is known to
precipitate arrhythmia; particular caution should
be taken to manage drug-drug interactions between commonly used COVID therapies and
antiarrhythmics and anticoagulants.
Does treatment for COVID-19 affect the use of
antiarrhythmic medications for AFib?
Drugs like chloroquine, hydroxychloroquine,
azithromycin, lopinavir and ritonavir used in the
management of COVID-19 can prolong the QT
interval. The effect of remdesivir on the QT
interval is unknown. AFib patients on
antiarrhythmic agents like dofetilide, sotalol,
amiodarone and dronedarone need careful
monitoring of the QT interval. When there is
significant QT prolongation and COVID treatment
is warranted, stopping antiarrhythmic medication
is reasonable if clinical circumstances allow.
Lopinavir-ritonavir combination increases serum
amiodarone (U.S. Food and Drug Administration
labeling recommends caution and monitoring of
serum amiodarone levels), digoxin and flecainide
levels. Similarly, chloroquine and
hydroxychloroquine can increase serum
amiodarone, digoxin and flecainide levels to a
lesser extent. Sotalol and dofetilide may need
dosing adjustments in COVID-19 patients with
acute kidney injury.
Does treatment for COVID-19 affect
anticoagulation for AFib?
Lopinavir-ritonavir combination (combined P-
glycoprotein/strong CYP3A4 inhibitor) can
potentially reduce warfarin levels and increase
apixaban, rivaroxaban and edoxaban levels. FDA
labelling suggests reducing apixaban dose to 2.5
mg twice daily if used concomitantly with
lopinavir-ritonavir combination. Consider
switching to alternate agents (preferably heparin or
enoxaparin).Chloroquine and hydroxychloroquine
can increase serum apixaban, dabigatran,
rivaroxaban and edoxaban levels. Close clinical
monitoring is required. Apixaban, dabigatran,
edoxaban and rivaroxaban may need dosing
adjustment in COVID-19 patients with acute
kidney injury.
How do you treat AFib in COVID-19 positive patients?
Where possible, a rate control strategy is
preferable, especially in critically ill patients who
can tolerate these medications. When
anticoagulation is indicated, use of heparin or
enoxaparin is preferable in patients where
chloroquine,hydroxychloroquine,lopinavir/ritona
vir use is anticipated. Antiarrhythmic drugs should
be used with caution due to the risk of QT
prolongation and drug-drug interactions with the
above-mentioned agents.
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What are thrombosis risk and management considerations in COVID-19?(4)
Despite the limited published evidence, most experts agree that the signal for increased thrombotic risk is sufficient to recommend
pharmacologic venous thromboembolism (VTE) prophylaxis in all hospitalized COVID-19 patients as long as there is no contraindication.
When clinically appropriate, a single daily low-
molecular weight heparin may help minimize staff
exposure risk and conserve personal protective
equipment (PPE).
The coagulopathy found in severe COVID-19
appears to be associated with normal or increased
fibrinogen levels, unlike disseminated
intravascular coagulopathy (DIC), and thus does
not present a clear increased risk for bleeding.
What is the link between hypertension and COVID-19? (5)
Although a causal relationship has not been
established, early epidemiological evidence suggests a correlation between hypertension and COVID-19 susceptibility and severity
• Initial reports from "hot spots" like Wuhan,
New York City, and the Lombardy region of
Italy found high rates of hypertension among
hospitalized COVID-19 patients.
• In a recent report, 56% of hospitalized
COVID-19 patients in a large New York
health care system presented with a diagnosis
of hypertension.
• In case series, patients with hypertension and
COVID-19 infection have higher rates of
morbidity and mortality.
• Many hospitalized COVID-19 patients are
older with multiple comorbidities; there is no
clear evidence of a causal link between
hypertension and COVID-19-related
morbidity and mortality.
• Hypertension remains the greatest
modifiable risk factor for atherosclerotic
cardiovascular disease.
• Clinicians should continue to follow the 2017
ACC/AHA blood pressure management
guidelines to reduce long-term cardiovascular
risk associated with hypertension.
What is the role of RAAS inhibitors in COVID-19? (6)
Currently there are no experimental or clinical
data demonstrating beneficial or adverse outcomes with background use of ACE inhibitors,
ARBs or other RAAS antagonists in COVID-19 or among COVID-19 patients with a history of cardiovascular disease treated with such agents.
• The HFSA, ACC, and AHA recommend
continuation of RAAS antagonists for those
patients who are currently prescribed such
agents for indications for which these agents
are known to be beneficial, such as heart
failure, hypertension, or ischemic heart
disease.
• In the event patients with cardiovascular
disease are diagnosed with COVID-19,
individualized treatment decisions should be
made according to each patient's
hemodynamic status and clinical
presentation.
• Therefore, be advised not to add or remove
any RAAS-related treatments, beyond
actions based on standard clinical practice.
What is the role of BNP measurement in
COVID-19? (7)
Natriuretic peptides are biomarkers of myocardial
stress are frequently elevated among patients with
severe respiratory illnesses, typically in the
absence of elevated filling pressures or clinical
heart failure.
• Much like troponin, elevation of BNP or NT-
proBNP is associated with an unfavorable
course among patients with ARDS.
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What is the role of troponin measurement in COVID-19? (8)
Troponin is commonly elevated in patients
COVID-19 and does necessarily indicate
myocardial infarction (MI) or other cardiac
sequalae; routine monitoring of troponin is
indicated upon clinical suspicion of MI or cardiac
dysfunction.
• Rise and/or fall of troponin – indicating
myocardial injury – is common among
patients with acute respiratory infections and
correlates with disease severity.
• Abnormal troponin values are common
among those with COVID-19 infection
particularly when a high sensitivity cardiac
troponin (hs-cTn) assay is used.
• Detectable hs-cTn is observed in most patients
with COVID-19 and significantly elevated in
more than half of the patients who died.
• The mechanisms underlying myocardial
injury in those with COVID-19 infection are
not fully understood.However in keeping with
other severe respiratory illnesses, direct ("non-
coronary") myocardial damage is almost
certainly the most common cause.
• Given the presence of abundant distribution of
ACE2 – the binding site for the SARS-CoV-2
in cardiomyocytes – some have postulated that
myocarditis might be a common cause.
• Support for this comes from reports of
COVID-19-related acute left ventricular
failure. Other possibilities include acute MI –
either Type 1 MI based on plaque rupture
triggered by the infection or Type 2 MI based
on supply-demand inequity.
• Importantly, a rise and/or fall of troponin is
insufficient to secure the diagnosis of acute
MI; rather, it should be based on clinical
judgment, symptoms and signs, and ECG
changes.
• Given the frequency and nonspecific nature of
abnormal troponin results among patients with
COVID-19 infection, clinicians are advised to
only measure troponin if the diagnosis of acute
MI is being considered on clinical grounds.
• In addition, an abnormal troponin should not
be considered evidence for an acute MI
without corroborating evidence.
What are some considerations for echocardiography in COVID-19? (9)
Echocardiography is an essential imaging
modality to assess cardiac complications of viral
infection as well as manage COVID+ patients with
underlying cardiovascular disease. However, in
the context of infectious disease, modifications of
standard procedure may be warranted.
Point-of-care ultrasound (POCUS) may be
advisable for COVID positive patients because it
allows in-room patient evaluation while
minimizing staff exposure.
How to image? Here is a suggested abbreviated ECHO protocol for COVID -19 patients (10)
Subcostal Long Axis
-2D Image
- Color Doppler of Mitral Valve and Tricuspid valve
-CW Doppler of Tricuspid valve if possible
Subcostal Short Axis
-IVC Diameter
-2DShort Axis of LV at Papillary level (for LV
function)
-2D Subcostal short axis
-Color Doppler of Tricuspid valve
- CW Doppler of Tricuspid valve if possible
Apical 4 Chamber
-2D Image
2D of LV ( zoomed or not, depending on image
quality) with focus on EF.
-3D Heart Model if images are adequate.
-Color Doppler of Mitral valve and Tricuspid valve
- CW Doppler of Tricuspid valve.
Apical 5 Chamber
-2D Image
-Color Doppler of Aortic valve
- CW Doppler of Aortic valve.
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Apical 2 Chamber
-2D Image
-2D of LV (zoomed or not, depending on image
quality) with focus on EF.
-Color Doppler of Mitral valve only if suspected
severe MR.
Apical 3 Chamber
-2D Images
- Color Doppler and CW Doppler of Aortic valve
only if suspected severe AS or AI.
No Images from the PLAX (parasternal long axis)
or PSAX (parasternal short axis).
TEEs carry a heightened risk of spread of the
SARS-CoV-2 since they may provoke
aerosolization of a large amount of virus due to
coughing or gagging that may result during the
examination.
TEEs therefore deserve special consideration in
determining when and whether they should be
performed, and under what precautions (described
below). A cautious consideration of the benefit of
a TEE examination should be weighed against the
risk of exposure of healthcare personnel to
aerosolization in a patient with suspected or
confirmed COVID-19 and the use of PPE. TEEs
should be postponed or canceled if an alternative
imaging modality (e.g. off axis TTE views,
ultrasound enhancing agent with TTE) can provide
the necessary information.
Protection
Personnel Imaging should be performed
according to local standards for the prevention of
virus spread. The types of PPE can be divided into
levels or categories (see Table below).
• Standard care involves handwashing or hand
sanitization and use of gloves. The use of a
surgical face mask in this setting may also be
considered.
• Droplet precautions include gown, gloves,
headcover, facemask and eye shield.
• Airborne precautions add special masks (e.g.
N-95 or N-99 respirator masks, or powered air purifying respirator - PAPR systems), and
shoe covers. The local application of each
component of PPE can vary according to
level or type of risk for TTEs and stress echo
exams, but airborne precautions are required
during a TEE for suspected and confirmed
cases, due to the increased risk for
aerosolization. A surgical face mask for
patients is recommended for those who are
symptomatic, undergoing surface echo
examination provided institutional resources
allow this strategy for source control.
Suggested algorithm for determining
indication and level of protection
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COVID-19 CORTICOSTEROID GUIDANCE | 06.18.20 @1800
Dexamethasone Updated 6/18/20 Potent anti-inflammatory and weak mineralocorticoid effects compared to other steroids. Long duration of action provides convenient dosing regimen.
Investigator-initiated, multicenter, RCT in 17 ICUs across Spain from March 2013-December 2018. Intubated and mechanically ventilated adults with early, moderate-to-severe, ARDS were included. Intervention group saw decreased ventilator days (12.3 vs. 7.5), ICU mortality, and all-cause mortality at day 60. In the multi-center adaptive RCT, Randomized Evaluation of COVID-19 Therapy (RECOVERY) trial, an interim analysis of 2104 patients randomized to receive dexamethasone were compared to 4321 patients randomized to usual care. Dexamethasone reduced deaths by one-third in ventilated patients and one fifth in patients on oxygen only, correlating with an NNT of 8 ventilated patients and 25 patients on supplemental oxygen. Full details of the trial are still pending peer-review and publication.
Dexamethasone 20 mg daily for five days, then 10 mg daily for days six through ten. Continued dexamethasone for a total of ten days, unless extubated prior to day ten. Then, dose was given prior to extubation and then stopped. Dexamethasone 6mg one daily (IV or PO) for 10 days
Potency of steroid and therefore possibility for steroid induced adverse effects are possible. Starting dose in this study dexamethasone 20 mg IV daily = methylpred 100 mg = prednisone 130 mg = hydrocortisone 500 mg
COVID-19 ANTIVIRAL GUIDELINES | 06.18.20 @1800
Pharmacy and Therapeutics Clinical Consensus Group COVID-19 Antiviral Medication Treatment Guidelines
June 18, 2020
Supportive Care is first line therapy for treatment of COVID19
Antiviral Medication Treatment • No FDA approved antivirals for COVID-19
• Several antivirals and immunomodulators are being investigated
• Information on safety and efficacy for COVID-19 is evolving with new literature released regularly
• Banner recommendations based on current literature, drug availability and disease severity o Recommendation to limit use of antiviral therapy to clinical trials where feasible
Remdesivir Treatment Guidelines • The U.S. Food and Drug Administration (FDA) has issued an Emergency Use Authorization (EUA) to permit the emergency
use of the unapproved product remdesivir for treatment of COVID-19. See EUA fact sheet for providers at https://www.fda.gov/media/137566/download
• Distribution of remdesivir for EUA is managed by HHS and the State Health Departments with limited availability
• Criteria developed to allocate and prioritize based on limited availability and allocation process outlined below
• Criteria in alignment with EUA and State of AZ released Remdesivir Allocation Guidance Approved by State Disaster
Medical Advisory Committee 6/12/20.
Emergency Authorization Criteria for Use
Prioritization Respiratory Criteria Recommendation
Inclusion Criteria: COVID PCR positive + Respiratory Criteria
Exclusion Criteria:
• ALT ≥ 5 times the upper limit of normal (ALT > 300)
• Patients with an eGFR < 30 ml/min including patients on HD or hemofiltration
Requirements for Use:
• Provider should discuss remdesivir and provide fact sheet to patients/ caregivers prior to administering med. (Available in Krames)
• Report all serious adverse events to FDA
Highest Priority
Respiratory Support* (3 of 4 characteristics) SpO2 < 94% on room air Initiation of supplemental oxygen Respiratory Rate >30 Lung infiltrates on imaging
• 200 mg IV Day #1, then 100 mg IV daily days 2-5 (5-day course)
Second Highest Priority
Invasive Mechanical Ventilation** or Patients on ECMO (Mechanical Ventilation and/or ECMO for 5 days or less)
• 200 mg IV Day #1, then 100 mg IV daily days 2-10 (10-day course)
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COVID-19 ANTIVIRAL GUIDELINES | 06.18.20 @1800
Hydroxychloroquine Guidelines
• The US Food and Drug Administration has revoked its emergency use authorization for the drugs hydroxychloroquine and chloroquine for the treatment of Covid-19
• Use of hydroxychloroquine for COVID-19 should be avoided unless given l in a clinical trial.
• If used outside of a clinical trial, the provider must review with patient/family the associated risks including increased incidence of adverse cardiac events and increased mortality.
• If provider determines benefit clearly outweighs risk, o Can consider Hydroxychloroquine (HCQ) 400 mg PO BID x 2 doses, then 200 mg PO BID x 4 days o Use with caution in patients with cardiac history o Avoid use in patients on other QT prolonging meds including azithromycin and levofloxacin o Obtain baseline ECG o Daily ECG or continuous cardiac monitoring with QTc capture every shift during course of therapy o QT monitoring as outlined below
QT Monitoring for Hydroxychloroquine
Initiation • Discontinue and avoid all other non-critical QT prolonging agents
• Complete list of medications that can prolong QT available at crediblemeds.org
• Assess baseline QTc, renal function, hepatic function, serum potassium, calcium and magnesium;
• Replace electrolytes (target potassium > 4 and magnesium > 2)
• Contact provider if baseline QTc > 500 msec (550 msec if baseline QRS width is >120 msec)
Monitoring • Baseline 12-lead ECG prior to initiation of therapy
• Monitor QTc via cardiac monitor in order to minimize staff exposure and PPE utilization
• For patients with prolonged QTc or borderline via monitor, a 12 lead ECG could be considered
• Assess QTc 2-3 hours after 1st dose and then every 24 hours during course of therapy
QT Prolongation • Assess potassium, calcium and magnesium; replace electrolytes and magnesium as needed
• Review medications and discontinue all other non-critical QT prolonging agents
• If QTc increases by > 60 msec from baseline or absolute QTc becomes > 550-570 (If baseline QRS is > 120 msec, then add 50 msec to these recommendations for discontinuation)
o Re-evaluate the risk/benefit of therapy o Consider discontinuing azithromycin (if receiving) o Consider discontinuation of HCQ if on alone and monitor QTc until returns to baseline
• If QTc remains increased despite discontinuation of azithromycin, consider discontinuing therapy
• If therapy is stopped due to QTc prolongation, re-challenging a patient may be considered if benefit is thought to be greater than the risk.
o Restart hydroxychloroquine 200 mg BID once QTc returns to baseline and monitor with QTc with each dose. (Note: long elimination half-life of hydroxychloroquine similar to amiodarone)
Brady and long QT • See COVID-19 toolkit for treatment recommendations.
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COVID-19 Related Medication Treatment Summary Adapted from Assessment of Evidence for COVID-19-Related Treatments. Bethesda, MD: American Society of Health-System Pharmacists, Inc.
Medication Class Comments Banner Recommendation
Antivirals
Baloxavir Antiviral No data to date support use in the treatment of COVID-19 Not recommended
Chloroquine Phosphate
Antimalarial
Active in vitro against SARS-CoV1 and SARS-CoV-2. Limited clinical data published. Multiple clinical trials initiated. Chloroquine is suggested a possible option in some international guidelines for treatment of COVID-19 but currently not recommended as first line therapy at BH given drug availability and published data. One trial in Brazil halted because of safety concerns with higher dosing regimens (600 mg bid).
Not recommended
Favipiravir Antiviral Benefit is uncertain given mixed result in trials. Clinical trials ongoing. Investigational agent not available in the US.
Not recommended/ Not available in US
Darunavir/Cobicistat HIV Protease Inhibitor
HIV-1 protease inhibitor currently being evaluated in a clinical trial (NCT04252274). There is one in vitro study that shows no activity against SARS-CoV-2 at clinically relevant doses.
Not recommended
Hydroxychloroquine Antimalarial
Active in vitro against SARS-CoV, MERS-CoV2, and SARS-CoV-2. Small studies have been done, most without a comparator group, small number of patients, and lower quality of evidence. Thus, it is difficult to infer benefit. There have been a couple studies in patients with mild disease that have shown positive results (viral clearance, possible efficacy cough relief, temperature normalization, and CT improvement in patients with mild disease). Four studies found no difference between groups in regards to negative conversion rate, ICU transfers, death, advancing to ARDS and LOS. Lastly, there has been concerns raised with HCQ use in hospitalized pts and oxygen requirements. Those pts did have higher baseline requirements. Dosing between studies has not been consistent. Based on study results, there is no clear evidence that this therapy provides benefit. It may benefit pts with more mild disease, but it is unknown at this time which pt population it is best suited for and what dose is optimal. This medication has the best availability within Banner. It could be considered on a risk vs. benefit assessment on a case by case basis. QTc monitoring is recommended if used as QT prolongation has been seen in studies and within our health system.
Not recommended A risk vs. benefit assessment should be done prior to initiation if therapy is desired. If therapy is ordered, recommended dose is HCQ 400 mg bid X 2 doses, then 200 mg bid X 4 days. QTc monitoring should be done. It is not recommended for use with azithromycin. See P & T Guidelines
Ivermectin Antiparasitic Only been shown in one in study to inhibit viral replication in vitro. No clinical trials currently or use in COVID-19 patients.
Not recommended
Lopinavir/Ritonavir (LPV/RTV; Kaletra®)
HIV Protease Inhibitor
Given the lack of therapeutic benefit seen in studies, use is not recommended at this time.
Not recommended
Neuraminidase inhibitors (e.g., oseltamivir)
Antiviral No data to date to support use in the treatment of COVID-19. Not recommended
Nitazoxanide Antiprotozoal Currently no known published clinical data regarding efficacy or safety in the treatment of COVID-19.
Not recommended
Remdesivir Antivirals, Miscellaneous
ACTT Trial showing faster time to recovery in patients receiving remdesivir than placebo but no overall difference in mortality. In addition, there has been additional data published showing no difference in 10 days of therapy versus 5 days in severe non intubated patients. Emergency use authorization issued. Currently, Banner Health has received a limited supply of remdesivir for use. Please see P&T criteria for use. Compassionate use is still available for pediatric and pregnant patients.
See P&T guidelines for criteria for use
Umifenovir (Arbidol®)
Antiviral Currently not available in the United States. Studies show mix results when compared to lopinavir/ritonavir. No data to support its use in COVID-19.
Not recommended/ Not available in US
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References
1. ACC, SCAI, ACEP Release Consensus Statement on
Management of AMI Patients During COVID-19 https://www.acc.org/latest-in cardiology/articles/20 20/04/29/12/42/key-questions-faq-on-covid-19-coronavirus-disease-2019-and-cardiovascular-disease#eleven
2. Management of the Hospitalized COVID-19 Patient with Acute Cardiomyopathy or Heart Failure https://www.acc.org/latest-in-cardiology/articles /2020/04/29/12/42/key-questions-faq-on-covid-19-coronavirus-disease-2019-and-cardiovascular-disease#seven
3. Bharath Rajagopalan, MD, FACC; Rachel Lampert, MD, FACC; Dhanunjaya Lakkireddy, MD, FACC. Managing AFIB during COVID-19 https://www. acc. org/latest-in-cardiology/articles/2020/04/29/12 /42/key-questions-faq-on-covid-19-coronavirus-disease-2019 -and-cardiovascular-disease#sixteen
4. Thrombosis and COVID-19: FAQs for Current Practice. https://www.acc.org/latest-in-cardiology /articles /2020/04/29/12/42/key-questions-faq-on-covid-19-coronavirus-disease-2019-and-cardiovascular disease#ten
5. Eugene Yang, MD, FACC; Anandita Agarwala, MD; Lisa Martin, MD, FACC; Arjun Kanwal, MD; Eileen Handberg, PhD, FACC https://www.acc.org/latest-in-cardiology/articles/2020/04/29/12/42/key-quest ions-faq-on-covid-19-coronavirus-disease-2019-and-cardiovascular-disease#seven
6. HFSA/ACC/AHA Statement Addresses Concerns Re: Using RAAS Antagonists in COVID-19 https://www. acc.org/latest-in-cardiology/articles/2020/03/17/08 /59/hfsa-acc-aha-statement-addre sses-concerns-re-using-raas-antagonists-in-covid-19
7. Troponin and BNP use in COVID-19. https://www. acc.org/latest-in-cardiology/articles/ 2020/04/29/12 /42/key-questions-faq-on-covid-19-coronavirus-disease-2019-and-cardiovascular-disease#one
8. Troponin and BNP use in COVID-19. https://www. acc.org/latest-in-cardiology/articles/2020/04/29/12 /42/key-questions-faq-on-covid-19-coronavirus-disease-2019-and-cardiovascular-disease#one
9. Source: ASE Statement on Protection of Patients and Echocardiography Service Providers During the 2019 Novel Coronavirus Outbreak https://www.acc.org /latest-incardiology/articles/2020/04/06/18/10/acc-endorses-ase-statement-on-echocardiography-protection-for-patients-providers-during-covid-19
10. https://www.asecho.org/covid-19-resources 11. Pharmacy and Therapeutics Clinical Consensus Group
COVID-19 Medication Treatment Guidelines June18, 2020, Banner Healthcare System, Arizona, USA. ( Corticosteroid and antiviral)
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Sri Lankan Journal of Cardiology Volume 3: Issue 2 - June 2020
COVID-19 and Acute Coronary Syndromes: Implications
and considerations F. Aaysha Cader
Assistant Professor & Associate Consultant, Department of Cardiology
Ibrahim Cardiac Hospital & Research Institute, Dhaka
E- mail: [email protected]
Declared a pandemic by the World Health Organization (WHO) in March 2020, the severe acute respiratory syndrome coronavirus 2
(SARS-CoV2) not only causes a viral pneumonia but has major implications for the cardiovascular system, with presentations ranging
from myocardial injury to myopericarditis, arrhythmia and acute coronary syndromes (ACS). A significant portion of patients with
Coronavirus disease 2019 (COVID-19) have elevated cardiac biomarkers, and may represent an acute myocardial injury with a variety
of aetiologies. As such, one needs to differentiate a Type I acute myocardial infarction (AMI) due to plaque rupture versus myocarditis,
stress cardiomyopathy, coronary spasm, or Type II AMI due to supply-demand mismatch. Given its robust capacity for human-to-human
transmission and potential of being a nosocomial source of infection, COVID-19 has specific implications on healthcare systems and
health care professionals, faced with performing essential cardiac procedures in patients with a suspected or confirmed diagnosis of
COVID-19. The primary goals in delivering emergency medical care during a pandemic are to ensure the efficient and time-appropriate
delivery of emergency services especially in cases such as ST-segment elevation myocardial infarction (STEMI), and in doing so, to
also limit the transmission of infection among healthcare workers and other in-hospital patients. The challenges to timely reperfusion
strategies ACS, and the decision-making between fibrinolysis and primary percutaneous coronary intervention (PCI) are multifold,
particularly in hospitals that may be unusually burdened at the height of the COVID-19 pandemic, where timely door-to-balloon time
may not be ensured, or where invasive procedures in a cardiac catheterization laboratory were limited by the absence of provision for
negative pressure ventilation. This is particularly applicable to resource-constrained healthcare systems, further compounded by the
additional challenges of unavailability of widespread on-site testing for SARS-CoV2. This article provides a brief overview of the
pathophysiology and cardiovascular implications of COVID-19 with a particular emphasis on pathways of care pertaining to ACS.
Keywords: COVID 19, Acute Coronary syndromes, CVD, RAS
The actual prevalence of ACS in the setting of
COVID-19 infection is unknown, given the gaps
in testing witnessed in numerous countries in the
early phases of the pandemic, and particularly in
the absence of typical symptoms suggesting
COVID-19 infection (2). Especially in this absence
of data, ACS during the pandemic deserves special
attention not only due to the susceptibility of
SARS-CoV2-infected patients, but also owing to
the urgency of its diagnosis and rapid institution of
prompt revascularization strategies.
The pathophysiology of ACS in COVID-19
The pathobiology of coronavirus infection
involves the binding of SARS-CoV‑2 to the host
receptor angiotensin-converting enzyme 2 (ACE2)
which mediates its entry into cells (7). ACE2,
which is expressed in the lungs, heart and
vasculature, is a key member of the renin
angiotensin system (RAS) important in the
pathophysiology of CVD (4, 7, 10, 11). The effects of
SARS-CoV2 on the heart and the vasculature
possibly result from a combination of direct and
indirect injury. Several mechanisms of the
interplay in the pathophysiology of the cardio-
respiratory effects of SARS-CoV2 infection,
including its immunological effects have been
proposed, some of which are depicted in Figure 1.
Introduction
The Coronavirus disease 2019 (COVID-19)
pandemic, caused by severe acute respiratory
syndrome coronavirus-2 (SARS-CoV-2) has
6,057,853 confirmed cases and claimed over
371,166 lives globally, as of 1st June 2020 (1).
Although the clinical picture of COVID-19 has
been dominated by the respiratory system, serious
cardiovascular consequences, including
myocardial injury, myocarditis, acute coronary
syndromes (ACS), arrhythmias, heart failure,
cardiogenic shock, deep vein thrombosis and
pulmonary embolism have been attributed to the
disease process caused by SARS-CoV2 (2-6).
Furthermore, it is becoming increasingly evident
that patients with pre-existing cardiovascular
diseases (CVD), particularly hypertension,
coronary artery disease (CAD) and
cardiomyopathy appear to have heightened
vulnerability to develop COVID-19 and a
tendency to more severe disease with worse
outcomes (2,4,7). Prior data demonstrate that
patients with acute respiratory infections were at
increased risk for subsequently developing acute
myocardial infarction (AMI) after both influenza
and non-influenza viral illnesses, including other
coronavirus species (8) , with fatal AMIs being
observed in the short term after coronavirus
associated SARS (9).
Ab
stra
ct
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Increased cardiac stress due to an increased
cardiometabolic demand associated with the
systemic infection coupled with hypoxia caused by
acute respiratory illness can impair myocardial
oxygen demand-supply relationship leading to
acute myocardial injury and a consequent type II
MI (5,6,10) .
Myocardial injury versus acute coronary syndromes
Myocardial injury is defined by an elevated cardiac
troponin (cTn) value (17), and can be due to
myocardial ischemia or non-ischemic myocardial
injury, which may arise secondary to myocarditis
or may be associated with non-cardiac conditions (17). Acute myocardial injury, manifest by an
increased level of biomarkers is not infrequently
encountered in COVID19 patients: the overall
incidence has been variable. However, initial
reports from China revealed that a considerable
proportion of patients (12-28%) presented elevated
cTn levels (10, 12, 14, 18-20). Elevated cTn levels have
been found to be a significant predictor of poor
outcomes and even mortality in multiple studies (18,19).
Shi et al. reported that 19.7% of the 416 patients
studied had cardiac injury defined as high
sensitivity troponin I greater than 99th percentile
upper reference limit. 57 of the 416 patients died,
of whom 10.6% had CAD.
The mechanisms of acute cardiac injury among
those infected with SARS-CoV2 are not well
established. One possible mechanism could be its
affinity to ACE2, which is widely expressed in the
heart, and cause direct myocardial injury (2, 4, 7, 10).
Direct infection of endothelial cells or pericytes
could lead to macrovascular or microvascular
dysfunction and downstream ischemic
consequences, as they express ACE-2 receptors to
which SARS-CoV2 bind directly (10, 11) .
In case of ACS or AMI, these pathophysiologic
effects could be further compounded by the
increased coagulability arising from systemic
inflammatory response and the ensuing cytokine
storm, as evidenced by significantly elevated
markers of coagulation, particularly D-dimer levels (6, 12-15).
Furthermore, immune over-reactivity along with
immunometabolism alterations could potentially
destabilize atherosclerotic plaques contributing to
development of acute coronary events (4).
Underlying this risk are the known predisposing
factors related to systemic inflammation:
endothelial and smooth muscle cell activation;
macrophage activation and tissue factor expression
in atheromatous plaque; and platelet activation
with further elaboration of inflammatory mediators (6, 16), all of which, combined with as increased
shear stress due to increased coronary blood flow
may potentially contribute to plaque rupture,
resulting in ACS (5, 16).
Figure 1: Pathophysiology of the cardio-respiratory effects of SARS-CoV2 infection
Infographic with kind permission of Professor Luigi P. Badano,
Professor of Cardiovascular Medicine, University of Milano-Bicocca, Milano, Italy.
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Sri Lankan Journal of Cardiology Volume 3: Issue 2 - June 2020
Where biomarkers are altered, a Type 2 MI may be
suggested in such cases. Patients with ACS do,
however, experience the more typical symptoms
related to ischaemia.
Among 28 COVID-19 patients with STEMI in
Lombardy, Italy, 78.6% presented with typical
chest pain associated or not associated with
dyspnea, while 21.4% had dyspnea without chest
pain (22).
Furthermore, cardiac patients may present with
out-of-hospital cardiac arrest or cardiogenic shock,
arising as a complication of either myocarditis or
ACS, necessitating an early, accurate, and rapid
evaluation to differentiate its aetiology (4, 21, 23).
Such patients should ideally be transferred and
further managed in expert centres which may offer
different choices of mechanical circulatory support (21). An additional differential diagnosis to be borne
in mind is acute pulmonary embolism, especially
given the increased tendency to hypercoagulability
in COVID-19 (15).
Early on during the pandemic, cardiologists across
the globe noted a drastic reduction in the numbers
of ACS presentation, most notably STEMIs
presenting to the emergency rooms. Garcia et al, in
a preliminary analysis during the early phase of the
COVID pandemic showed an estimated 38%
reduction in cardiac catheterization laboratory
STEMI activations in the United States (24) , similar
to the 40% reduction noticed in Spain (25) . Tanner,
et al, in an elegant paper, detailed potential
contributory factors to this reduction, namely
altered patient behavior, disrupted care pathways,
or altered cardiovascular risk factors pertaining to
partial or complete lockdown conditions (26). It also
detailed the challenges to cardiology services
which may arise from decreased or delayed STEMI
presentations, especially medium and long-term
complications such as heart failure and sudden
cardiac death as well as clinical consequences of
the un-revascularized cohort (26).
The presentations of ACS in COVID-19 have been
variable. Before published case series and reports
emerged, social media was rife with anecdotes of
the so-called “COVID STEMIs”, some of which
presented with typical ECG changes but yielded no
thrombotic occlusions on coronary angiography.
These findings proved to be consistent with
published data, emerging not soon after. Stefanini,
et al, reported that among 28 STEMI patients with
COVID-19 in Lombardy, Italy, STEMI
represented the first clinical manifestation of
COVID-19 in the majority (85.7%) of cases (22) .
Moreover, in multivariable adjusted models,
cardiac injury was significantly and independently
associated with mortality (19) .
Similarly, Guo et al., reported myocardial injury
with elevated troponin T levels in 28% of the 187
patients studied. 35% had underlying CVD.
Mortality was significantly higher among those
with high cTn levels versus those with normal cTn
(59.6% vs 8.9% respectively, p<0.001) (18).
Circulating cTn is a marker of myocardial injury,
including but not limited to myocardial infarction
(MI) or myocarditis, are commonly elevated in
hospitalized patients, and are as likely to be due to
non-ischemic causes of myocardial injury or type 2
MI (myocardial oxygen supply-demand
imbalance), than as a consequence of ACS (20) .
Furthermore, cTn elevations in patients with
COVID-19 infection seem to be lower than in most
cases of ACS or acute myocarditis and adequate
attention paid to alternate diagnoses such as
myocarditis, Takotsubo syndrome, spontaneous
coronary dissection, or a type 2 MI (21) . The use of
coronary angiography for COVID-19-positive
patients with elevation in cTn should be restricted
to those in whom type 1 MI is suspected (21).
Given this range of differential diagnoses of
elevated cTn levels in COVID-19 patients, and the
distinctly poorer outcomes associated with it, it is
imperative that a clear distinction and prompt
diagnosis of ACS (i.e. myocardial ischaemia) be
made, so as to urgently facilitate appropriate
management and revascularization.
Patterns of ACS presentation in COVID-19
This requires recognizing the patterns of
presentation of ACS, which is not without
challenges, considering the significant overlap in
symptoms of ACS with initial presentations of
COVID-19, in addition to reports of suggestive ST
elevations on electrocardiogram (ECG) eventually
revealing non-obstructive coronary arteries on
angiography.
The symptom of chest pain or tightness is common
in patients with active COVID-19 infection, is
usually poorly localized and may be associated
with breathlessness due to the underlying
pneumonia (4). Furthermore, an associated
profound hypoxaemia together with tachycardia
may result in chest pain and accompanying
electrocardiographic changes suggestive of
myocardial ischaemia (4) .
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Sri Lankan Journal of Cardiology Volume 3: Issue 2 - June 2020
She was intubated shortly after presentation due to
hypoxic respiratory failure and managed
conservatively with angiography deferred, given
active COVID-19 infection. Reverse Takotsubo
syndrome associated with COVID-19 has also been
reported in the literature (31) .
Given the magnitude of such COVID STEMIs, and
the need for data and shared learning, a COVID
ACS Registry by the University of Glasgow on
behalf of the University Hospitals of Leicester
NHS Trust is currently collecting data via an audit
web portal, to enable better understanding of how
the COVID-19 virus is affecting those with ACS (32) .
Challenges in delivery of ACS care during the pandemic
The primary goals in delivering emergency
medical care during a pandemic essentially
requires the efficient and time-appropriate delivery
of emergency services, especially in cases such as
STEMI, and in doing so, to also limit the
transmission of infection among healthcare
workers and other in-hospital patients.
In addition to patient-related delays in presentation,
ensuring timely door-to-balloon times could prove
to be challenging given the additional burden of
COVID-19 cases, particularly in resource-
constrained hospital setting. While this is
particularly true for cases of coexistent COVID-19
and ACS, the limitations to reliable on-site rapid
testing preclude the possibilities of confidently
“ruling out” SARS-CoV2 in persons under
investigation (PUI) as well. This is further
compounded by the presence of STEMI
“mimickers’”, particularly those with STEMI-like
ECG changes and more commonly, the
accompanying elevated troponin levels with a
consequent need to differentiate them from true
ACS (21, 28) .
The importance of point of care ultrasound
(POCUS), or targeted screening echocardiography
looking for regional wall motion abnormalities
cannot be understated, especially in presentations
of STEMI, where cath lab activation for primary
PCI is of essence (23, 27 ). Given that chest CT is
frequently used to confirm COVID-19 pneumonia,
this might provide possible synergies of and
opportunities for cardiac imaging (21) .
Early mortality was 39.3%. All patients underwent
urgent coronary angiography and 60.7% had
evidence of a culprit lesion requiring
revascularization, while 39.3% had no obstructive
coronary artery disease.
Bikdeli and colleagues, in a case series of 18 STEMI
presentations in New York, reported similar
angiographic findings, with 67% of obstructive
disease among the 9 patients who underwent
angiography (27) . In that series, 10 out of 18 were
identified as noncoronary myocardial injury on the
basis of either nonobstructive coronaries on
angiography or normal wall motion on
echocardiography (if angiography was not done).
Furthermore, 4 (22%) of the patients had diffuse ST
elevations on ECG, all of whom subsequently had
non-obstructive coronaries on angiography. This
also underscores the need for paying special
attention to the ECG prior to cath lab activation: the
absence of reciprocal ST depression, presence of PR
segment depression, global ST elevations involving
more than a single coronary artery territory are all
possible markers indicating that the case many not
be one of obstructive coronary artery disease (28) .
The 8 patients (44%) in the New York case series
who received a clinical diagnosis of STEMI also
had higher median peak troponin and d-dimer levels
than those with noncoronary myocardial injury.
Overall, in-hospital mortality, was high, at 72%,
with 9 of the deaths occurring from among the 10
patients with noncoronary myocardial injury (27) .
Dominguez-Erquicia and colleagues from Spain
reported the case of multivessel ‘in situ’ coronary
thrombosis, in a 64-year-old with no prior risk
factors who presented with STEMI, one week after
being discharged with COVID-19 pneumonia but
no anticoagulation therapy (29). A critical thrombotic
stenosis of the proximal right coronary artery was
stented with a drug eluting stent after thrombus
aspiration. A non-occlusive filling defect of the left
anterior descending (LAD) artery was confirmed to
be thrombus without underlying atherosclerotic
plaque on optical coherence tomography of LAD,
which was managed medically with dual antiplatelet
therapy (DAPT) and heparin.
A case of Takotsubo Syndrome, consistent with
classic findings on echocardiography including
apical ballooning in a 58-year old diabetic woman
was reported by Minhas, et al., possibly the first
such case report of stress cardiomyopathy in the
setting of COVID-19 (30) . She had presented with a
five-day history of productive cough, fever and
diarrhea, with diffuse ST segment elevations on
ECG and apical ballooning on echocardiography.
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Nevertheless, in cases of STEMI with low risk of
COVID-19, primary PCI remained the preferred
strategy with immediate transfer to the cardiac
catheterization laboratory (33,34) .
Guidelines by the Cardiological Society of India
(CSI) have recommended primary PCI as the
preferred strategy for confirmed or suspected
COVID-19 patients presenting with STEMI within
12 hours, if performed with the necessary
precautions, especially if the patient is
haemodynamically unstable. In case of
hemodynamically stable patients in whom PCI may
not be feasible, thrombolysis has been
recommended (36).
National Health Service (NHS) guidelines from the
United Kingdom also reiterate that primary PCI
should be delivered as the default therapy for
patients with pain of <12 hours and ST elevation,
with specific guidance to manage left bundle
branch block (LBBB) in local hospitals unless the
patient has ongoing intractable pain (37) .
Thrombolysis, while not preferred for STEMI, may
be considered on a case-by-case basis for unstable
patients with coronavirus pneumonia who develop
a STEMI (37) .
A joint consensus statement from Society for
Cardiovascular Angiography and Interventions
(SCAI), American College of Cardiology (ACC),
and the American College of Emergency
Physicians (ACEP) echoed the general consensus
that primary PCI remains the standard of care for
STEMI patients at PCI capable hospitals when it
can be provided in a timely fashion, with an expert
team outfitted with PPE in a dedicated cath lab. A
fibrinolysis-based strategy may be entertained at
non-PCI capable referral hospitals or in specific
situations where primary PCI cannot be executed
or is not deemed the best option (23) .
As for COVID positive or probable cases
presenting with NSTEMI, the overwhelming
consensus from different guideline documents is in
favour of a conservative strategy of medical
management, especially given that the majority of
NSTEMI patients do not have ongoing ischaemia
and respond well to medical treatment, allowing
time to test the patients for COVID-19 infection (21,23,37) . However, they may be taken for urgent
coronary angiography and possible PCI in the
presence of high-risk clinical features (Global
Registry of Acute Coronary Events (GRACE)
score >140)20 or hemodynamic instability (21,34) .
As such, it can be considered to integrate the
protocol alongside CT coronary angiography, in
order to exclude or confirm an ACS, particularly
non-ST segment myocardial infarction (NSTEMI)
in COVID-19 pneumonia where elevated cTn are
common (21,33,34) . Bedside chest radiography can be
considered an alternative to chest CT for rapid
exclusion of pulmonary infiltrates in patients (33) .
Pathways of care in STEMI: Primary PCI versus thrombolysis
In case of STEMI, an early reperfusion may be
more important than the mode of reperfusion (35) .
Timely primary PCI relies heavily on systems of
care, not just individual operators. System delays
in the provision of care of primary PCI during the
COVID-19 era arise, even among COVID-19
negative patients, through the steps and time in the
emergency room required to establish contact
history, symptomatology, chest X ray and other
investigations prior to transfer to the cardiac cath
lab. Cath lab staff require time to don personal
protective equipment (PPE) and may perform their
usual roles slower (35) . Healthcare systems at the
height of the pandemic may have stretched out
resources, and in such scenarios, a single bolus
fibrinolytic in the emergency room may be a
feasible alternative (35) .
Various healthcare systems in different countries
across the globe have recommended their approach
to treatment of STEMI in the setting of COVID-19
pandemic (21,23,33,34,36-38) .The basis for choosing
between primary PCI and fibrinolysis as the default
treatment strategy has been primarily based on
speed of activating cath lab in order to maintain
door-to-wire times, rapid availability of primary
PCI operators and presence of catheterization
laboratories with negative pressure ventilation (34,35) .
At the inception of the pandemic, Chinese
protocols predominantly favoured emergency
intravenous thrombolysis within 30 minutes as the
first choice for acute STEMI in cases with
confirmed COVID-19, in absence of
contraindications to fibrinolysis (33,34) . The
emphasis was on minimal transmission of infection
to healthcare workers (HCWs) with patients being
kept in strict isolation until rapid COVID-19
screening tests became available, for those with
suspected COVID-19 (33,34) .
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Sri Lankan Journal of Cardiology Volume 3: Issue 2 - June 2020
Conclusion
As more data becomes available, given the
dynamicity of the pandemic, there may be a
constant need to reassess the risk-benefit ratio of
optimal management strategies across the spectrum
of ACS, weighing in the effect of different stages
of the pandemic on hospital preparedness and the
potential availability of rapid testing. Going
forward, it is also imperative that mass public
education efforts by means of various media be
encouraged, in order to assure patients that
healthcare services remain operational and safe for
use, especially in case of acute cardiovascular
conditions like STEMI, where time-sensitive
treatment pathways exist, and delayed
presentations could lead to catastrophic
consequences.
Acknowledgement
The author acknowledges Professor Luigi P.
Badano, Professor of Cardiovascular Medicine,
University of Milano-Bicocca, Milano, Italy for his
kind permission for use of the infographic on the
pathophysiology of the cardio-respiratory effects
of SARS-CoV2 infection used in this manuscript.
References
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Safety of healthcare workers and considerations for cardiac catheterization laboratory
Given its highly contagious nature with proximity
dependent spread and viability in aerosols for hours
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all cases (21) .
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7. Chapman AR, Bularga A, Mills NL. High-Sensitivity Cardiac Troponin Can Be An Ally in the Fight Against COVID-19 [published online ahead of print, 2020 Apr 6].Circulation. 2020;10.1161/CIRCULATIONAHA.120.047008. doi:10.1161/CIRCULATIONAHA.120.047008
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14. Bangalore S, Sharma A, Slotwiner A, et al. ST-Segment Elevation in Patients with Covid-19 - A Case Series [published online ahead of print, 2020 Apr 17]. N Engl JMed.2020;NEJMc2009020. doi:10.1056/NEJMc2009020
15. Deshpande A, Birnbaum Y. ST-segment elevation: Distinguishing ST elevation myocardial infarction from ST elevation secondary to nonischemic etiologies. World J Cardiol. 2014;6(10):1067‐1079. doi:10.4330/wjc.v6.i10.1067
16. Dominguez-Erquicia P, Dobarro D, Raposeiras-Roubín S, Bastos-Fernandez G, Iñiguez-Romo A. Multivessel coronary thrombosis in a patient with COVID-19 pneumonia, European Heart Journal, ehaa393, https://doi.org/10.1093/eurheartj/ehaa393
17. Minhas AS, Scheel P, Garibaldi B, et al. Takotsubo Syndrome in the Setting of COVID-19 Infection [published online ahead of print, 2020 May 1]. JACC Case Rep. 2020;10.1016/j.jaccas.2020.04.023. doi:10.1016/j.jaccas.2020.04.023
18. Sala S, Peretto G, Gramegna M, et al. Acute myocarditis presenting as a reverse Tako-Tsubo syndrome in a patient with SARS-CoV-2 respiratory infection, Eur Heart J 2020; 41(19): 1861–1862, https://doi.org/10.1093/eurheartj/ehaa286
19. Zheng YY, Ma YT, Zhang JY, et al. COVID-19 and the
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20. Kwong JC, Schwartz KL, Campitelli MA. Acute Myocardial Infarction after Laboratory-Confirmed Influenza Infection. N Engl J Med. 2018; 378: 2538-2541
21. Peiris JS, Chu CM, Cheng VC, et al. Clinical progression and viral load in a community outbreak of coronavirus-associated SARS pneumonia: a prospective study. Lancet 2003;361(9371):1767-72. https://doi.org/10.1016/s0140-6736(03)13412-5
22. Tersalvi G, Vicenzi M, Calabretta D, Biasco L, Pedrazzini G, Winterton D. Elevated Troponin in Patients With Coronavirus Disease 2019: Possible Mechanisms [published online ahead of print, 2020 Apr 18]. J Card Fail. 2020;S1071-9164(20)30357-2. doi:10.1016/j.cardfail.2020.04.009
23. Chen L, Li X, Chen M, et al. The ACE2 expression in human heart indicates new potential mechanism of heart injury among patients infected with SARS-CoV-2. Cardiovascular Research 2020. https://doi.org /10.1093/cvr/cvaa078
24. Zhou F, Yu T, Du R, et al. Clinical course and risk factors for mortality of adult inpatients with COVID-19 in Wuhan, China: a retrospective cohort study. Lancet. 2020; DOI: 10.1016/S0140-6736(20)30566-3. [epub ahead of print].
25. Madjid M, Safavi-Naeini P, Solomon SD, et al. Potential Effects of Coronaviruses on the Cardiovascular System: A Review [published online ahead of print, 2020 Mar 27]. JAMA Cardiol. 2020;10.1001/jamacardio.2020.1286. doi:10.1001/jamacardio.2020.1286
26. Huang C, Wang Y, Li X, et al. Clinical features of patients infected with 2019 novel coronavirus in Wuhan, China. Lancet. 2020;395:497-506.
27. Bikdeli B, Madhavan MV, Jimenez D, et al. COVID-19 and Thrombotic or Thromboembolic Disease: Implications for Prevention, Antithrombotic Therapy, and Follow-up. J Am Coll Cardiol. 2020 Apr 15:S0735-1097(20)35008-7
28. Libby P, Simon DI. Inflammation and thrombosis: The clot thickens. Circulation. 2001;103:1718-1720
29. Thygesen K, Alpert JS, Jaffe AS, et al. Fourth Universal Definition of Myocardial Infarction (2018). Glob Heart. 2018;13(4):305‐338. doi:10.1016/j.gheart. 2018.08.004
30. Guo T, Fan Y, Chen M, et al. Cardiovascular Implications of Fatal Outcomes of Patients With Coronavirus Disease 2019 (COVID-19). JAMA Cardiol 2020. https://doi.org/10.1001/jamacardio.2020.1017
31. Shi S, Qin M, Shen B, et al. Association of Cardiac Injury With Mortality in Hospitalized Patients With COVID-19 in Wuhan, China [published online ahead of print, 2020 Mar 25]. JAMA Cardiol. 2020;e200950. doi:10.1001/jamacardio.2020.0950
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32. Study: COVID ACS Registry.
https://www.rcbweb.com/COVIDACSREG_de2/login.aspx?ReturnUrl=%2fCOVIDACSREG_de2%2f (Accessed on 1st June 2020)
33. Jing ZC, Zhu HD, Yan XW, et al. Recommendations from the Peking Union Medical College Hospital for the management of acute myocardial infarction during the COVID-19 outbreak. Eur Heart J. 2020;41(19):1791‐1794. doi:10.1093/eurheartj/ehaa258
34. Han Y, Zeng H, Jiang H, et al. CSC Expert Consensus on Principles of Clinical Management of Patients with Severe Emergent Cardiovascular Diseases during the COVID-19 Epidemic. Circulation. 2020 Mar 27. doi: 10.1161/CIRCULATIONAHA.120.047011.
35. Daniels MJ, Cohen MG., Bavry AA, et al. Reperfusion of STEMI in the COVID-19 Era – Business as Usual?. Circulation. 2020. 10.1161/CIRCULATIONAHA. 120.047122
36. Kerkar PG, Naik N, Alexander T, et al. Cardiological Society of India: Document on Acute MI care during COVID-19. Indian Heart J. 2020 May 6. doi: 10.1016/j.ihj.2020.04.009. Epub ahead of print. PMCID: PMC7201231.
37. Speciality guides for patient management during the coronavirus pandemic. Clinical guide for the management of cardiology patients during the coronavirus pandemic 20 March 2020 Version 1. https://www.england.nhs.uk/coronavirus/wp-content/ uploads/sites/52/2020/03/specialty-guide-cardiolgy-coronavirus-v1-20-march.pdf (Accessed on 11th April 2020)
38. Zhang L, Fan Y, Lu Z. Experiences and lesson strategies for cardiology from the COVID-19 outbreak in Wuhan, China, by 'on the scene' cardiologists. Eur Heart J. 2020;41(19):1788‐1790. doi:10.1093/eurheartj/ehaa266
39. Figure legend: Figure 1: Pathophysiology of the cardio-respiratory effects of SARS-CoV2 infection Infographic with kind permission of Professor Luigi P. Badano, Professor of Cardiovascular Medicine, University of Milano-Bicocca, Milano, Italy.
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`
Rapid Journal Scan From the Editorial desk
Iron deficiency in worsening heart failure is associated with reduced estimated protein intake, fluid retention, inflammation, and antiplatelet use. Haye H. van der Wa et al.
European Heart Journal (2019) 40, 3616–3625
Iron deficiency (ID) is common in heart failure
(HF) patients and negatively impacts symptoms
and prognosis. The aetiology of ID in HF is largely
unknown. This study investigated determinants
and the biomarker profile of ID in a large
international HF cohort.
The data suggest that the aetiology of ID in
worsening HF is complex, multifactorial and
seems to consist of a combination of reduced iron
uptake (malnutrition, fluid overload), impaired
iron storage (inflammation, chronic kidney
disease), and iron loss (antiplatelets).
What is the optimal blood pressure? Differences between current guidelines and novel insights into kidney injury Thomas F. Lϋscher.
European Heart Journal (2019) 40, 3443-3446
Guidelines are highly important, and the European
Society of Cardiology and European Society of
Hypertension (ESC/ ESH1), as well as their US
counterparts2 regularly publish such guidelines.
Whilst agreeing on many points, there are also
important differences in the recommendations of
these three guidelines, one such difference being
the target blood pressures which are 120 mmHg
systolic in the US Guidelines, 120–129 mmHg for
younger and 130– 139 mmHg systolic for elderly
hypertensives in the ESC Guidelines, and still
140/90 mmHg in the conservative NICE
Guidelines (Table 1).
The kidney is a major target organ of damage in
HT.
A comprehensive analysis of the effects of rivaroxaban on stroke or transient ischaemic attack in patients with heart failure, coronary artery disease, and sinus rhythm: the COMMANDER HF trial
Mandeep R. Mehra et al.
European Heart Journal (2019) 40, 3593–3602
Stroke is often a devastating event among patients
with heart failure with reduced ejection (HFrEF).
In COMMANDER HF, rivaroxaban 2.5 mg b.i.d.
did not reduce the composite of first occurrence of
death, stroke, or myocardial infarction compared
with placebo in patients with HFrEF, coronary
artery disease (CAD), and sinus rhythm. The study
examines the incidence, timing, type, severity, and
predictors of stroke or a transient ischaemic attack
(TIA), and seek to establish the net clinical benefit
of treatment with low-dose rivaroxaban.
In this double-blind, randomized trial, 5022
patients who had HFrEF(<_40%), elevated
natriuretic peptides, CAD, and who were in sinus
rhythm were treated with rivaroxaban 2.5 mg b.i.d.
or placebo in addition to antiplatelet therapy, after
an episode of worsening HF.
Conclusions
Patients with HFrEF and CAD are at risk for stroke
or TIA in the period following an episode of
worsening heart failure in the absence of atrial
fibrillation. Most strokes are of ischaemic origin
and nearly half are either disabling or fatal.
Rivaroxaban at a dose of 2.5 mg b.i.d. reduced
rates of stroke or TIA compared with placebo
in this population.
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Sri Lankan Journal of Cardiology Volume 3: Issue 2 - June 2020
Thus, biomarkers of kidney tubule injury,
inflammation, and fibrosis have been studied
extensively and suggested to be associated with
cardiovascular outcomes.
The article entitled ‘Markers of kidney tubule
function and risk of cardiovascular disease events
and mortality in the SPRINT trial investigated this
issue in more depth in 2377 hypertensives with
chronic kidney disease of the SPRINT trial.
association.
Unadjusted, α1 and ß2 microglobulin had positive
associations with major cardiovascular events
(MACE), whereas uromodulin had an inverse
association.
In multivariate analysis including estimated
glomerular filtration rate (eGFR) and albuminuria,
a two-fold higher baseline concentration of a1
microglobulin was associated with higher risk of
MACE and mortality, whereas ß2 microglobulin
had no associations.
A two-fold higher uromodulin concentration was
associated with lower MACE, with a hazard ratio
of 0.79, but not mortality after adjusting for
confounders.
The ESC/ESH guidelines reiterate the importance
of reducing blood pressure (BP) below 140/90
mmHg for all patients, but go further to suggest,
where tolerated, that systolic blood pressure (SBP)
for those aged under 65 should be reduced to
between 120 and 129 mmHg.
The updated NICE guideline continues to
recommend treating to a threshold and target BP
of 140/90 mmHg, as opposed to the lower
treatment targets recommended by the ESC/ESH.
To understand how such differences can occur
between the NICE and ESC/ESH guidelines, it is
necessary to recognize that they use two different
processes with different aims and methods.
NICE produces government-funded national
guidelines intended for population treatment based
on both clinical evidence and cost-effective
analysis. NICE start with a series of questions,
which can be quite specific, based on feedback
from a broad range of stakeholders. ESC and ESH
are medical societies who fund the clinical
guideline development, with a broad scope,
intended for treatment of individuals in many
European countries with different socio-economic
populations.
The evidence base and its interpretation also
differed within each guideline, which had
implications for recommendations. This
fundamental difference in interpretation is
exemplified by the SPRINT trial.
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Sri Lankan Journal of Cardiology Volume 3: Issue 2 - June 2020
Sex differences in heart failure Carolyn S P Lam et al. European Heart Journal (2019) 40, 3859–3868
The overall lifetime risk of heart failure (HF) is
similar between men and women, however, there
are marked sex differences in the landscape of this
condition that are both important and under-
recognized.
Men are predisposed to HF with reduced ejection
fraction (HFrEF), whereas women predominate in
HF with preserved ejection fraction (HFpEF).
Sex differences are also notable in the penetrance
of genetic cardiomyopathies, risk factors, e.g.
breast cancer which may be associated with cancer
treatment-induced cardiomyopathy, as well as sex-
specific conditions such as peripartum
cardiomyopathy (PPCM).
A central hypothesis is that the higher risk of
HFrEF in men compared to women may be
attributable to their predisposition to
macrovascular coronary artery disease and
myocardial infarction, whereas coronary
microvascular dysfunction/endothelial
inflammation has been postulated to play a key
role in HFpEF and maybe the common link among
HF syndromes that women are predisposed to
Takotsubo cardiomyopathy, PPCM, and breast
cancer radiotherapy-induced cardiomyopathy.
Under-pinning current sex disparities in HF, there
is a paucity of women recruited to HF clinical trials
(20–25% of cohorts) and thus treatment guidelines
are predominantly based on male-derived data.
Large gaps in knowledge exist in sex-specific
mechanisms, optimal drug doses for women and
sex-specific criteria for device therapy.
NICE considered that the methodology of
measuring BP could not be translated into UK
clinical practice and so did not lower the
recommended treatment target. The use of
automated devices set on a time delay, with an
unaccompanied rest period, is not common
practice in the UK and was considered likely to
result in significantly lower BP readings than those
taken in routine clinical practice.
Gender in cardiovascular medicine: chest pain and coronary artery disease Puja K Mehta et al. European Heart Journal (2019) 40, 3819–3826
Ischaemic heart disease (IHD) remains the leading
cause of morbidity and mortality among women
and men yet women are more often
underdiagnosed, have a delay in diagnosis, and/or
receive suboptimal treatment.
An implicit gender-bias with regard to lack of
recognition of sex-related differences in
presentation of IHD may, in part, explain these
differences in women compared with men.
Existing knowledge demonstrates that angina does
not commonly relate to obstructive coronary artery
disease (CAD). Emerging knowledge supports an
inclusive approach to chest pain symptoms in
women, as well as a more thoughtful consideration
of percutaneous coronary intervention for angina
in stable obstructive CAD, to avoid chasing our
tails.
Emerging knowledge regarding the cardiac
autonomic nervous system and visceral pain
pathways in patients with and without obstructive
CAD offers explanatory mechanisms for angina.
Interdisciplinary investigation approaches that
involve cardiologists, biobehavioural specialists,
and anaesthesia/pain specialists to improve angina
treatment should be pursued.
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Sri Lankan Journal of Cardiology Volume 3: Issue 2 - June 2020
NZOTACS—New Zealand Oxygen Therapy in Acute Coronary Syndromes trial
ESC Congress 2019
The role—and benefits or harm—of oxygen in
acute coronary syndrome has been uncertain, with
ESC guidelines recommending oxygen in patients
with STEMI and non-STEMI when blood oxygen
saturation is below 90%, but not routinely above
this level. Additionally, the possibility of harm in
non-hypoxaemic patients was raised by a 2018
meta-analysis.
The aim of the New Zealand Oxygen Therapy in
Acute Coronary Syndromes (NZOTACS) trial was
to identify or exclude modest favorable or adverse
effects of oxygen in non-hypoxaemic or mildly
hypoxaemic patients with a suspected or
confirmed acute coronary syndrome.
The cluster randomized crossover trial compared
two oxygen protocols as part of routine care in 40
872 patients over 2 years. The primary endpoint
was 30-day mortality obtained from a national
database. For all patients, 30-day mortality was the
same with the high and low oxygen protocols
(3.1% vs. 3.0%).
Principal investigator Professor Ralph Stewart of
Green Lane Cardiovascular Service, Auckland
City Hospital, New Zealand, said: ‘This suggests
that oxygen is neither beneficial nor harmful, and
it is safe to give oxygen to patients presenting with
a suspected or confirmed acute coronary
syndrome’. For patients with STEMI, 30-day
mortality was significantly decreased with the high
compared to the low oxygen protocol (8.8% vs.
10.6%). However, Prof. Stewart added that while
oxygen may benefit patients presenting with
STEMI, who have the most severe myocardial
ischaemia and the highest mortality, more
evidence is needed to be sure.
The COMPLETE (COMPLETE Revascularization with Multivessel Percutaneous Coronary Intervention in ST-segment Elevation Myocardial Infarction) trial. ESC Congress 2019
The international randomized COMPLETE trial
showed that complete revascularization reduces
major cardiovascular events, compared to culprit-
lesion only PCI.
About half of patients with ST-segment elevation
myocardial infarction (STEMI) have multivessel
coronary artery disease (CAD). This means that in
addition to the culprit artery, they have additional
stenosed (non-culprit) coronary arteries. In STEMI
patients, opening the culprit artery with PCI
reduces cardiovascular death or myocardial
infarction. It is unclear whether additional PCI of
non-culprit lesions also prevents these events.
‘The question of whether to routinely
revascularize non-culprit lesions or manage them
conservatively with guideline-directed medical
therapy alone is a common dilemma’.
For the study, 4041 patients with STEMI and
multivessel CAD were enrolled from 140 centres
in 31 countries with patients randomly allocated to
complete revascularization with additional PCI of
angiographically significant non-culprit lesions, or
to no further revascularization. At a median
follow-up of 3 years, the first coprimary outcome
of cardiovascular death or myocardial infarction
occurred in 158 patients (7.8%) in the complete
revascularization group compared to 213 (10.5%)
in the culprit-lesion only group. The second co-
primary outcome of cardiovascular death,
myocardial infarction, or ischaemia-driven
revascularization occurred in 179 patients (8.9%)
in the complete revascularization group compared
to 399 (16.7%) in the culprit-lesion only group.
‘COMPLETE is the first randomized trial to show
that complete revascularization reduces hard
cardiovascular events compared to culprit-lesion
only PCI in patients with STEMI and multivessel
coronary artery disease.
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Sri Lankan Journal of Cardiology Volume 3: Issue 2 - June 2020
Safety and efficacy outcomes of double vs. triple antithrombotic therapy in patients with atrial fibrillation following percutaneous coronary intervention: a systematic review and meta-analysis of non-vitamin K antagonist oral anticoagulant-based randomized clinical trials Giuseppe Gargiulo et al.
European Heart Journal (2019) 40, 3757–3767
Aims were to investigate the safety and efficacy of
double vs. triple antithrombotic therapy (DAT vs.
TAT) in patients with atrial fibrillation (AF) and
acute coronary syndrome or who underwent
percutaneous coronary intervention (PCI).
A systematic review and meta-analysis was
performed using PubMed to search for non-vitamin
K antagonist oral anticoagulant (NOAC)-based
randomized clinical trials comparing DAT vs. TAT
in AF patients undergoing PCI.
The primary safety endpoint (ISTH major or
clinically relevant non-major bleeding) was
significantly lower with DAT compared with TAT,
which was consistent across all available bleeding
definitions. This benefit was counterbalanced by a
significant increase of stent thrombosis and a trend
towards higher risk of myocardial infarction with
DAT. There were no significant differences in all-
cause and cardiovascular death, stroke and major
adverse cardiovascular events.
Conclusion Double antithrombotic therapy,
particularly if consisting of a NOAC instead of
VKA and a P2Y12 inhibitor, is associated with a
reduction of bleeding, including major and
intracranial haemorrhages. This benefit is however
Counterbalanced by a higher risk of cardiac mainly
stent-related but not cerebrovascular ischaemic
occurrences.
Transcatheter Aortic Valve Implantation vs. Surgical Aortic Valve Replacement for Treatment of Symptomatic Severe Aortic Stenosis: An Updated Meta-Analysis.
George C M Siontis European Heart Journal (2019) 40, 3143-3153.
Owing to new evidence from randomized
controlled trials (RCTs) in low-risk patients with
severe aortic stenosis, this study compared the
collective safety and efficacy of trans-catheter
aortic valve implantation (TAVI) vs. surgical
aortic valve replacement (SAVR) across the entire
spectrum of surgical risk patients.
Conclusion: Compared with SAVR, TAVI is
associated with reduction in all-cause mortality
and stroke up to 2 years irrespective of baseline
surgical risk and type of THV system.
Impact of long-term ticagrelor monotherapy following 1-month dual antiplatelet therapy in patients who underwent complex percutaneous coronary intervention: insights from the Global Leaders trial Patrick W. Serruys et al.
European Heart Journal (2019) 40, 2595–2604
Aims were to evaluate the impact of an
experimental strategy [23-month ticagrelor
monotherapy following 1-month dual antiplatelet
therapy (DAPT)] vs. a reference regimen (12-
month aspirin monotherapy following 12-month
DAPT) after complex percutaneous coronary
intervention (PCI).
Conclusion was that ticagrelor monotherapy
following 1-month DAPT could provide a net
clinical benefit for patients with complex PCI.
However, in view of the overall neutral results of
the trial, these findings of a post hoc analysis
should be considered as hypothesis generating.
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Defining High Bleeding Risk (HBR) in Patients Undergoing Percutaneous Coronary Intervention:- A Consensus Document From the Academic Research Consortium for High Bleeding Risk Philip Urban et al. European Heart Journal (2019) 40, 2632–2653
Identification and management of patients at high
bleeding risk undergoing percutaneous coronary
intervention are of major importance, but a lack of
standardization in defining this population limits
trial design, data interpretation, and clinical
decision-making.
A consensus definition of patients at high bleeding
risk was developed that was based on review of the
available evidence.
Elevated high-density lipoprotein in adolescents with Type 1 diabetes is associated with endothelial dysfunction in the presence of systemic inflammation Scott T. Chiesaet al.
European Heart Journal (2019) 40, 3559–3566
High-density lipoprotein (HDL) function may be
altered in patients with chronic disease,
transforming the particle from a beneficial
vasoprotective molecule to a noxious pro-
inflammatory equivalent. Adolescents with Type 1
diabetes often have elevated HDL, but its
vasoprotective properties and relationship to
endothelial function have not been assessed.
Seventy adolescents with Type 1 diabetes (age 10–
17 years) and 30 age-matched healthy controls was
the study population.
HDL-c levels and glycated haemoglobin (HbA1c)
were increased in all patients compared with
controls. However, increased inflammation and
HDL dysfunction were evident only in patients
who also had evidence of early renal dysfunction.
Endothelial function (FMD) was impaired only in
those who had both a high inflammatory risk score
and high levels of HDL-c (P < 0.05).
Increased levels of HDL-c commonly observed in
individuals with Type 1 diabetes may be
detrimental to endothelial function when
accompanied by renal dysfunction and chronic
inflammation.
Dysfunctional HDL and inflammation is a noxious liaison in adolescents with type 1 diabetes Philipp Jakob al. European Heart Journal (2019) 40, 3567-3570
Diabetes mellitus is a key condition that fosters
pro-inflammatory, pro-apoptotic, and pro-
oxidative properties of HDL particles. Indeed,
HDL isolated from both patients with type 2
diabetes and those with T1DM show an impaired
anti-inflammatory capacity, despite comparable or
even elevated HDL levels in T1DM patients as
compared with healthy controls.
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Contrary to expectations, the loss of HDL-
associated vasculo-protective effects is not
confined to HbA1c or poor glycemic control,
suggesting that drivers other than elevated glucose
levels render HDL dysfunctional. In this respect,
inflammation and renal dysfunction have been
shown to change the functional and structural
properties of HDL.
The neurohormonal basis of pulmonary hypertension in heart failure with preserved ejection fraction
Masaru Obokata et al.
European Heart Journal (2019) 40, 3707–3717
Pulmonary hypertension (PH) represents an
important phenotype among the broader spectrum
of patients with heart failure with preserved
ejection fraction (HFpEF), but its mechanistic basis
remains unclear. The authors hypothesized that
activation of endothelin and adrenomedullin, two
counterregulatory pathways important in the
pathophysiology of PH, would be greater in
HFpEF patients with worsening PH, and would
correlate with the severity of haemodynamic
derangements and limitations in aerobic capacity
and cardiopulmonary reserve.
Plasma levels of C-terminal pro-endothelin-1 (CT-
proET-1) and mid-regional pro-adrenomedullin
(MR-proADM), central haemodynamics,
echocardiography, and oxygen consumption
(VO2) were measured at rest and during exercise
in subjects with invasively-verified HFpEF (n =38)
and controls free of HF (n=20) as part of a
prospective study.
Conclusion
Subjects with HFpEF display activation of the
endothelin and adrenomedullin neurohormonal
pathways, the magnitude of which is associated
with pulmonary haemodynamic derangements,
limitations in RV functional reserve, reduced
cardiac output, and more profoundly impaired
exercise capacity in HFpEF. Further study is
required to evaluate for causal relationships and
determine if therapies targeting these
counterregulatory pathways can improve outcomes
in patients with the HFpEF-PH phenotype.
Cardiovascular effect of discontinuing statins for primary prevention at the age of 75 years: a nationwide population-based cohort study in France
Philippe Giral et al. European Heart Journal (2019) 40, 3516–3525
The role of statin therapy in primary prevention of
cardiovascular disease in persons older than 75
years remains a subject of debate with little
evidence to support or exclude the benefit of this
treatment. We assessed the effect of statin
discontinuation on cardiovascular outcomes in
previously adherent 75-year-olds treated for
primary prevention.
This was a population-based cohort study using
French national healthcare databases was
performed, studying all subjects who turned 75 in
2012-14, with no history of cardiovascular disease
and with a statin medication possession ratio ≥80%
in each of the previous 2 years. Statin
discontinuation was defined as three consecutive
months without exposure.
Statin discontinuation was associated with a 33%
increased risk of admission for cardiovascular
event in 75-year old primary prevention patients.
Conclusion
The results of this study suggest potential
cardiovascular risk reduction associated with
continuing statin therapy after the age of 75 years
in persons already taking these drugs for primary
prevention. However, due to the observational
nature of this study, residual confounding cannot
be excluded. Future studies, including
interventional randomized studies, are needed to
confirm these findings and support updating and
clarification of guidelines on the use of statins for
primary prevention in the elderly.
As seen in the current study, early statin
discontinuation was associated with increased risk
of MI and CV death. The former US President Bill
Clinton actually experienced this. As he did rehab
for his knee, he exercised and lost weight, so he
stopped his statin, but a few months later
developed unstable angina and required coronary
bypass surgery.
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Conclusion
Individuals with CVD may benefit from physical
activity to a greater extent than do healthy subjects
without CVD.
This study from Korea is certainly limited by the
fact that this Asian population generally had much
better overall CVD profiles and maritedly lower
body mass indices and prevalence of obesity than
similar populations in the USA and most of
Europe. Also, this study analyzed only leisure-
time physical activity, which was self-reported.
This is in contrast to the emphasis in recent
guidelines which focus on all forms of physical
activity (household management. transportation,
etc., in addition to leisure-time physical activity) in
any time intervals (not just done in 10-min
intervals for CVD prevention.
Although not ensure-time physical activity and
cardiorespiratory fitness are associated with
substantial CVD protection, most studies
demonstrated that cardiorespiratory fitness is
considerably more powerful than physical activity
for protecting against CVD risk and mortality.
Finally there is now evidence that demonstrates
not only that physical activity/leisure-time
physical activity is important, but also that limiting
sedentary behavior and physical inactivity is also
extremely important for CVD protection, even
independently of physical activity.
We can contrast with aspirin for primary
prevention, where recent trials have shown
increased bleeding and no benefit in the elderly.14
An editorialist on one of these recent aspirin
studies, Dr. Paul Ridker, concluded ‘Thus, beyond
diet maintenance, exercise, and smoking cessation,
the best strategy for the use of aspirin in the
primary prevention of cardiovascular disease may
simply be to prescribe a statin instead’.
Mortality reduction with physical activity in patients with and without cardiovascular disease
Sang-Woo Jeong et al. European Heart Journal (2019) 40, 3547–3555
Physical activity has been shown to reduce
mortality in a dose-response fashion. Current
guidelines recommend 500–1000 metabolic
equivalent task (MET)-min per week of regular
physical activity. This study aimed to compare the
impact of leisure-time physical activity on
mortality in primary versus secondary
cardiovascular prevention.
This study included a total of 131 558 and 310 240
subjects with and without cardiovascular disease
(CVD), respectively, from a population-based
cohort. Leisure-time physical activity was
measured by self-report questionnaires. The study
subjects were followed-up for a median of 5.9
years, and the main study outcome was all-cause
mortality. There was an inverse relationship
between the physical activity level and the
mortality risk in both groups.
The benefit in the secondary prevention group was
shown to be greater than that in the primary
prevention group: every 500 MET-min/week
increase in physical activity resulted in a 14% and
7% risk reduction in mortality in the secondary and
primary prevention groups, respectively
(interaction P < 0.001).
In addition, while individuals without CVD
benefited the most between 1 and 500 MET-
min/week of physical activity, the benefit in those
with CVD continued above 500 - 1000 MET-
min/week. The adjusted mortality risk of
individuals with CVD who performed a high level
of physical activity (>_1000 MET-min/week) was
shown to be comparable to or lower than that of
their counterparts without CVD.
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COVID -19 Basics for Cardiologists From the editorial desk
1. What do the terms COVID 19 and SARS-
COV-2 signify?
The virus is called COVID-19.
The syndrome caused by it is called SARS-
COV-2. (SARS - Severe acute respiratory
syndrome)
The virus is a single stranded RNA virus.
It can survive on metal, glass and plastic surfaces
for a few days. Toys, utensils and mobile phones
fall into this category.
The virus can survive on cardboard, paper and
cotton clothing for a few days. Books, magazines
and paper money fall into this category.
Latex rubber gloves are not protective as the virus
can survive on them for few days.
The virus can last on ceramic ware, steel ware and
wood for few days. Door handles, taps, coins,
cupboard doors etc. fall into this category.
The term ‘a few days’ in the text above refers to
the long range of 3-9 days. This long range is given
in order to cover all published studies but 3days is
the usual period of survival.
The virus survives for 3 hours in the droplets
coughed out into air. (Now it is thought that even
normal talking can cause emission of such
droplets).
The emission of droplets is higher when you talk
forcefully in a noisy crowded area or in a loud
music background. Emission is also probably
higher when you sing aloud compared to quiet
talking.
Small droplets of 1-5 µm in diameter can float in
the air for 3 hours (and sometimes longer). These
are called aerosols.
If the atmosphere temperature is low, the virus can
persist as aerosol for 28 days.
New data suggests that the virus can be excreted in
the feces of a patient for weeks. Hence good
personal hygiene is essential for all patients and
close associates.
Washing with soap and water for 20 seconds
eliminates the virus.
Alcohol solutions (of 62-71%) will also eliminate
the virus in 20 seconds. (However for both the
above, a time period of 1 minute is suggested if
contamination is likely).
Much of the knowledge regarding COVID 19 virus
is still unconfirmed. Hence the above facts might
be revised with further insight into the virus.
2. Why was the safety of ACE-I and ARBs queried in SARS-COV-2 patients?
The COVID- 19 virus is single standard RNA
enveloped virus which has a structural spike (s)
protein which binds to the angiotensin converting
enzyme 2 (ACE 2) on cell membranes. After
binding to the ACE 2 the virus enters the cell. (At
present we know of no other way the virus can
enter a human cell).
3. What is ACE 2?
This is a member of the ACE family. (These are
dipeptidyl carboxydipeptidases). Angiotensin
converting enzyme 2 (ACE 2) is a close homolog
of the angiotensin converting enzyme commonly
called ACE. (which is blocked by the ACE
inhibitor drugs).
The actions of ACE and ACE 2 are different.
• ACE cleaves angiotensin I to angiotensin II.
The angiotensin I binds to angiotensin
receptor 1 (AT-1R) which causes
vasoconstriction and other effects which
lead to hypertension.
• ACE 2 cleaves angiotensin II and generates
angiotensin. This is a potent vasodilator and
also has anti-hypertrophic and anti-
inflammatory actions all of which are
beneficial.
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5. What will happen to the ACE system with COVID infection?
The COVID virus will bind to ACE 2. This will
affect the ACE / ACE 2 balance so that there will
be heightened angiotensin II activity.
This will lead to;
1. pulmonary vasoconstriction
2. pulmonary inflammation
3. oxidative organ (lung) damage
You may even postulate that the use of ACE-I or
ARB may lead to a mitigation of these deleterious
effects of angiotensin II.
But guidelines so far recommend the use of ACE-
I /ARB, ONLY for definite indications such as
hypertension, heart failure and diabetes.
6. What happens to ACE 2 when you treat with ACE-I ?
ACE inhibitors decrease levels of angiotensin II.
Hence there is an indirect upregulation of ACE 2
protein. (Angiotensin II is known to reduce ACE
2 expression).
Theoretically, patients on ACE-I will have a
greater number of ACE 2 protein on the cell
membrane, through which viral particles can enter
into human cells.
This is why ACE I were first suggested to be
inappropriate in COVID 19 infections.
7. What happens to ACE 2 when you treat with ARBs?
The clinically used ARBs are angiotensin I
receptor blockers.
ARBs augment free angiotensin II levels and
hence, theoretically at least, can lead to a reduction
in ACE-2 protein density. This will be beneficial
in COVID 19 infections.
• ACE 2 is a membrane protein (found on
cells of the lung, liver, testes, heart, kidney
and intestine).
• ACE 2 expression is increased in HT, HF as
a protective mechanism.
• Use of ARB blockers increases ACE 2
expression.
• Use of ACE-I may increase ACE 2
expression but this is controversial.
AT1R: angiotensin II type 1 receptor; AT2R:
angiotensin II type 2 receptor; MasR: Mas receptor;
SARS-CoV-2: severe acute respiratory syndrome
coronavirus 2. European Journal of Preventive Cardiology 0(0) 1–4
©The European Society of Cardiology 2020
4. Where do you find ACE 2?
We find it in most tissues but it is highly expressed
in the lung and heart. A high density of the ACE 2
is also found in the;
- intestine
- kidney
- blood vessels.
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8. Do we need to omit the ACE-I and ARB in patients already on them?
The current evidence based recommendation is
that these drugs may be continued when used as
guide line based therapy for another disease such
as HT, Heart failure, diabetes mellitus etc.
9. What is the status of neprilysin O inhibitor + angiotensin II receptor blocker combination (sacubitril / valsartan) in SARS-COV-2 ?
Because the COVID 19 virus uses the ACE 2 as a
receptor to bind to the cell membrane, in SARS -
COV-2 the ACE 2 levels are down regulated – so
that there is an increase in the production of
angiotensin. In this scenario sacubitril / valsartan
combination can be beneficial.
Hence it can be continued in COVID 19 infections.
10. How do I interpret the troponin I results in COVID 19 infected patients?
HS/Troponin I levels are elevated in most COVID-
19 positive patients. Significant rises are seen in
more than 50% of patients who die of COVID-19.
As the myocardium has a rich content of ACE 2 to
which COVID 19 binds, it’s quite possible that
myocardial damage occurs leading to HS-
Troponin elevation.
11. What are the usual troponin levels expected in SARS COV-2?
On admission (ie onset of symptoms):-
In survivors - .0025ng/ml
In non survivors - .0088ng/ml
During follow-up:-
In survivors - .0025-.0044 ng/ml
In non survivors -.25ng/ml and more
These values are mere approximations derived
from a single study.
12. How can I use troponin I levels to diagnose an acute coronary even in SARS COV 2 patients?
Because troponin rise is mostly ‘non specific’ in
COVID 19’ patients do not routinely assay the
troponin unless:
- clinical judgment
- symptoms and signs
- ECG changes
Suggest incident cardiac pathology.
Do not diagnose cardiac pathology based on the
troponin levels alone. Always use clinical
judgment, clinical features of ECG changes and
echo findings to diagnose any cardiac
involvement.
Even a rising titre of troponin will be non-
diagnostic in SARS-COV-2 unless other features
confirm the diagnose of ACS.
Note :- Do NOT routinely do troponin I testing in
COVID 19 infection.
This will only lead to increased ‘downstream
testing’ such as CT coronary angiography,
invasive angiography, cardiac nuclear studies and
cardiac MRI studies etc.. all of which are out of the
sphere of rational medicine in managing SARS-
COV-2.
13. What happens to BNP levels in COVID-19?
In many respiratory illnesses of some degree of
severity, BNP levels can rise- even though the LV
filling pressures are normal and there are no
clinical features of heart failure.
However, in ARDs, a rise in BNP signifies a bad
prognosis.
In COVID 19 positive patients too, BNP levels are
commonly elevated. This must not be construed as
heart failure without other clinical features and
echo cardiographic evidence of LV dysfunction.
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14. What mechanisms can explain the rise in biomarkers in SARS COV2 patients?
1. Direct viral damage of the myocytes.
2. Secondary damage due to hypoxia.
3. Systemic inflammation due to cytokine
storm.
15. Do troponin and BNP levels have a value in prognostication?
Yes: Both these cardiac markers signify a worse
prognosis specially if significantly elevated.
They can therefore be useful for prognostication
but not for firm diagnosis of ACS or heart failure.
16. What pathological processes can cause HF in SARS COV-2? 1. Viral myocarditis
2. Stress cardiomyopathy
3. Cytokine induced cardiomyopathy due to
cytokines storm. This is important to keep
in mind as dexamethasone will help these
patients.
17. Can a Brugada type ECG be seen in SARS-COV-2?
Remember that Brugada syndrome can be
unmasked in COVID 19 infections as in any
febrile illness.
18. What cardiac syndromes can occur in SARS- COV 2?
1. Viral myocarditis
2. Stress cardiomyopathy (typical takotsubo)
3. Acute coronary syndrome
4. Atrial fibrillation, VT, heart block and other
arrhythmias too
19. What co-morbidities affect COVID mortality?
Mortality is higher in
- diabetics
- hypertensives
These patients tend to develop a high density of
ACE 2 as a protective mechanism. This stands
against them in COVID 19 infections.
Hence cardiologists have to be vigilant in care of
these patients.
20. How did chloroquine and hydroxychloroquine enter the COVID discussion?
These drugs have been used for a long time in
managing malaria, SLE and rheumatoid arthritis.
These drugs affect host receptors, by various
chemical means and there by retard virus entry in
cells.
Although initial small studies were promising,
good data on the efficacy of these drugs in COVID
19 is lacking.
The interest to the Cardiologist is that these drugs
cause prolongation of the QT interval.
Correctly, the QTc must be measured before
administration these drugs for COVID patients.
However experienced physicians say that they
never checked / check QTc when using these drugs
for malaria.
21. Is it safe to combine hydroxy-chloroquine with azithromycin for COVID 19 patients?
This combination is no longer used. Both these
drugs prolong the QTc and combination of the two
may lead to cardiac emergencies.
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22. Can antiplatelet agents and anticoagulants be used in SARS-COV-2?
Thrombosis is probably common in COVID-19
infection due to
- excessive inflammation
- activation of platelets
- endothelial dysfunction
- blood stasis
The thrombotic process can occur in both arterial
and venous systems with organ ischaemia and
distal embolization.
Hence all patients already on antiplatelet agents
and anti-coagulants must continue on same if they
get infected with COVID 19.
Prophylaxis for venous thrombo embolism (VTE)
must not be routinely given in SARS-COV-2. You
need to follow the standard guidelines for this.
Prophylaxis for arterial and venous thrombosis is
given only if there is an incident episode of
thrombosis or the risk for thrombosis is very high.
Both heparin and enoxaparin can be used in
SARS-COV-2 as per usual guidelines.
23. Can amiodarone and verapamil be
used in COVID-19 patients?
Once the virus binds to the ACE 2, it enters the cell
by endocytosis.
Once within the cell the virus genome is released
into the host cytoplasm. This involves a long
process which apparently needs an acidic pH.
Drugs which are called cationic amphiphilic drugs
(CAD) reduce the acidic pH of the cell. These
drugs will therefore help retard viral proliferation
once inside the cell.
CADs are-
- amiodarone
- dronedarone
- verapamil
Hence these drugs can be used by the cardiologist
to treat arrthymias in COVID-19 infections.
24. What are the basic preventive measures to be taken by cardiologists? 1. Limit face to face contact:-
• Hence try to conduct virtual clinics.
In Sri Lanka the audio consultation
with the help of Viber or WhatsApp
is best as it is accessible for most
people.
• Auscultate minimally
• Limit 2Decho study to LV function
only
• Use once a day enoxaparin dosage to
avoid going near the patient too
frequently.
2. Avoid non urgent procedures.
Do not hesitate for an invasive procedure
in
- STEMI
-Very high risk and high risk NSTEMI
• Out of hospital cardiac arrest needs
an invasive procedure only if a
STEMI is present on ECG.
• Permanent pacing is to be done only
for symptomatic 3o, 2o heart blocks or
severe SSS.
• Have a ‘Hot’ or Dirty Cath lab /
theater dedicated for COVID
patients.
• For management of a cardiac arrest
where face-to –face contact cannot be
minimized, full aerosol generating
procedure PPE must be worn.
25. Is heparin safe in covid-19? Heparin binds onto the spike protein of cell
membranes and thus may prevent the virus
entering. It may be used with the usual
precautions.
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Sri Lankan Journal of Cardiology Volume 3: Issue 2 – June 2020
First patient was a 31 year old male navy officer
who was unable to take warfarin due to his
occupational risks of trauma and failed
radiofrequency ablation; second patient was a 71
year-old diagnosed patient with oesophageal
varices who had episodes of haematemesis; third
patient was a 51 year-old female with poor
compliance to OAC and erratic INR and fourth
patient was a 69 year old male patient with a
history of a deep intracranial bleed without
neurological deficit while on warfarin which was
managed successfully.
Transoesophageal echocardiography (TOE) was
done initially on all four selected patients to
exclude LA & LAA clots and to measure LAA
diameters. Diameters taken were of the LAA
orifice and the neck, 10 mm perpendicularly down
and parallel to orifice (Figure 1). TOE was also
done during the procedure and dimensions
measured to confirm and to decide the size of the
occluder. In all four patients right femoral venous
access was obtained with a 12F sheath. A 0.032-
inch guidewire was advanced to left subclavian
vein. The sheath was exchanged with an 8F
Mullins Sheath. The System was withdrawn to
right atrium and inter atrial septum (IAS) was
punctured more inferiorly with a Brockenbrough
needle under TOE and fluoroscopic guidance. A
5F Pig tail catheter was advanced through the
sheath into the LAA and demarcated with a
contrast injection (Figure 2)
Introduction
In patients with atrial fibrillation (AF), an
ischaemic stroke may occur as the initial
presenting manifestation due to formation of a
cardiac thrombus. Any form of AF (i.e.
paroxysmal, persistent, or permanent) can lead to
development and subsequent embolization of
atrial thrombi. Cardiac thrombi originating from
the LAA is the common cause (>90%) of
ischaemic stroke in AF patients (1,2). LAA is a
muscular pouch connected to the left atrium (LA)
of the heart. In AF patients, fibrosis and
inflammation seen in the LA are particularly
intense in the LAA and fibrillating LAA is the
only area within the left atrium that comprise of
pectinate muscle and can create an appropriate
milieu for blood stasis and thrombus formation.
Patients with non-valvular AF and high risk for
ischaemic stroke (CHA2DS2 VASc >2) should be
on an oral anticoagulant (OAC) for stroke
prevention. LAA device closure is an option for
patients who have clear contraindications, poor
compliance and are intolerant to OAC.
Case series
We selected four patients with non-valvular AF
(rate controlled) with CHA2DS2 VASc Score > 2
for this case series at Institute of Cardiology in
National Hospital of Sri Lanka on 9th November
2019.
A case series of Left Atrial Appendage (LAA)
Device closure in Sri Lanka
Ranasinghe WG1, Shetty R2, Paul VE3, Ponnamperuma CJ1, Paranamana
RS1, Karunarathne S1, Vithanage TDP1, Colombage DDE1, Sajeev S1,
Sovis WFRD1, Jayasinghe VP1, Liyanage HTRP1
1. Institute of Cardiology, National Hospital of Sri Lanka
2. Department of Cardiology, Kasturba Medical College, Manipal
3. Royal Perth Hospital, Australia
Corresponding author: Dr. Gotabhaya Ranasinghe, Consultant Cardiologist E-mail: [email protected]
Ab
stra
ct
Ischaemic stroke is a major complication in atrial fibrillation (AF) due to cardiac emboli. Most cardiac emboli in AF arise from
the left atrial appendage (LAA).
Oral anticoagulant (OAC) is widely used for stroke prevention in patients with risk of stroke in AF and the commonly used drug
is warfarin. Some patients may have contraindications, complications, intolerance and poor compliance to OAC. Percutaneous
LAA device closure is an evolving procedure which mechanically occludes the LAA reducing the usage of OAC and also stroke
events by preventing thrombus formation in the LAA. It is now recommended in guidelines for stroke prevention in patients with
AF who are unable to take warfarin. LAA device closure is non-inferior to OAC in stroke prevention.
Key words: Atrial fibrillation, Left atrial appendage, Stroke, Oral anticoagulation
.
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The pigtail catheter was removed and a Judkins
Right (JR) catheter was introduced into left
superior pulmonary vein (LSPV) over an extra
stiff guidewire. The Mullins sheath was removed
with the wire left in LSPV. The Amplazter
Amulet LAA occluder (22, 28, 25 & 25 mm
devices respectively) was introduced over the
wire. The System was withdrawn to the LAA
orifice with the lobe of the device slightly
deployed. The device was deployed after
confirming the position with TOE and
fluoroscopy (Figure 3). Post-deployment contrast
injection did not show any peri-device leak
(Figure 4).
After 6 months, all four patients were reviewed in
the Cardiology follow up clinic and found to have
no new complaints, history of any embolic events,
palpitations and all were haemodynamically
stable with rate-controlled AF.
Figure 1: TOE image of LAA at 450 and diameters of
the orifice and neck of LAA
Figure 2: Angiographic image of LAA
Figure 3: Deployment of the Amplazter Amulet LAA
occluder.
Figure 4: Post procedure LA angiography shows no
leak of contrast in to LAA.
Discussion
OAC use for stroke prevention in patients with AF
has various disadvantages and complications
including serious haemorrhages leading to death.
Most commonly used OAC in Sri Lanka is
warfarin which needs regular INR monitoring,
strict compliance and has various interactions
with food and drugs.
In patients who are unable to take OAC, other
non-pharmacological approaches such as
radiofrequency ablation does not seem to reduce
embolic risk. Since the LAA is the common
source of thrombi in AF (90%), percutaneous
device closure or surgical exclusion is non-
inferior to OAC for stroke prevention in AF
patients with moderate stroke risk (3,4,10).
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However 10% of the emboli are not from the
LAA, and hence LAA device closure will not
completely prevent stroke in AF patients (2). The
European society of cardiology (ESC)
recommends LAA percutaneous device occlusion
for non-valvular AF patients with stroke risk and
clear contraindications for OAC (7).
Amplatzer Amulet LAA occluder is the second
generation Amplatzer LAA device made on
proven Amplatzer technology and has significant
advantages, including wider lobe and more
stabilizing wires (up to 10 pairs) for improved
device stability, and larger lobe size to occlude
larger appendages(5). This is the second
commonest device to be used in LAA device
closure worldwide after Watchman LAA device.
Conclusion Major cause of ischaemic stroke in patients with
AF is cardiac emboli arising from LAA. Long
term anticoagulation is recommended in patients
with AF and high stroke risk (7). Patients who are
unable to take or having contraindications to
taking OAC, LAA appendage occlusion with
device is an option to prevent stroke (7).
Carrying out similar procedures regularly in the
near future is being planned now and it will be
available soon as a procedure of choice for
patients having problems with OAC.
References 1. Stöllberger C, Schneider B, Finsterer J. Elimination of
the left atrial appendage to prevent stroke or embolism? Anatomic, physiologic, and patho-physiologic considerations. Chest, 2003; 124(6): 2356‐2362. doi:10.1378/chest.124.6.2356.
2. Blackshear JL, Odell JA. Appendage obliteration to reduce stroke in cardiac surgical patients with atrial fibrillation. Ann Thorac Surg, 1996; 61: 755.
3. Reddy VY, Sievert H, Halperin J, et al. Percutaneous Left Atrial Appendage Closure vs Warfarin for Atrial Fibrillation: A Randomized Clinical Trial. JAMA, 2014; 312(19): 1988–1998. doi: 10.1001/jama.2014.15192
4. Holmes DR Jr, Doshi SK, Kar S, et al. Left Atrial Appendage Closure as an Alternative to Warfarin for Stroke Prevention in Atrial Fibrillation: A Patient- Level Meta-Analysis. J Am Coll Cardiol, 2015; 65(24): 2614‐2623. doi: 10.1016/j.jacc. 2015. 04.025
5. Meier B, Palacios I, Windecker S, et al. Transcatheter left atrial appendage occlusion with Amplatzer devices to obviate anticoagulation in patients with atrial fibrillation. Catheter Cardiovasc Interv 2003; 60: 417.
6. Landmesser U, Schmidt B, Nielsen-Kudsk JE, et al. Left atrial appendage occlusion with the AMPLATZER Amulet device: periprocedural and early clinical/ echocardiographic data from a global prospective observational study. EuroIntervention 2017; 13: 867.
7. Paulus Kirchhof, Stefano Benussi, Dipak Kotecha, Anders Ahlsson, Dan Atar, Barbara Casadei, Manuel Castella, Hans-Christoph Diener, Hein Heidbuchel, Jeroen Hendriks, Gerhard Hindricks, Antonis S Manolis, Jonas Oldgren, Bogdan Alexandru Popescu, Ulrich Schotten, Bart Van Putte, Panagiotis Vardas, ESC Scientific Document Group, 2016 ESC Guidelines for the management of atrial fibrillation developed in collaboration with EACTS, European Heart Journal, 7 October 2016; 37(Issue 38): 2893-2962. https://doi.org/10.1093/ eurheartj/ehw210
8. Sievert H, Lesh MD, Trepels T, et al. Percutaneous left atrial appendage transcatheter occlusion to prevent stroke in high-risk patients with atrial fibrillation: early clinical experience. Circulation, 2002; 105: 1887.
9. Ostermayer SH, Reisman M, Kramer PH, et al. Percutaneous left atrial appendage transcatheter occlusion (PLAATO system) to prevent stroke in high- risk patients with non-rheumatic atrial fibrillation: results from the international multi-center feasibility trials. J Am Coll Cardiol, 2005; 46: 9.
10. Holmes DR, Reddy VY, Turi ZG, et al. Percutaneous closure of the left atrial appendage versus warfarin therapy for prevention of stroke in patients with atrial fibrillation: a randomised non-inferiority trial. Lancet, 2009; 374: 534.
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Myocardial infarction with non-obstructive coronary arteries (MINOCA) is the terminology currently used to describe patients
presenting with clinical symptoms of myocardial infarction without fixed obstructions in epicardial coronary arteries. Epicardial and
micro vascular coronary artery spasms are known causes in above category. Vascular endothelial dysfunction also contributes to the
above clinical entity. Coronary artery spasm is a functional disorder, which is caused by intense, reversible obstruction of coronary
arteries. We report a case of a patient presenting with acute anterior STEMI complicated with ventricular tachycardia requiring
cardioversion to the emergency department. His coronary angiogram showed diffuse stenotic segments in both left anterior descending
and circumflex arteries. Those coronary artery obstructions were improved with intra coronary administration of GTN. Thus we
objectively diagnosed epicardial coronary artery spasms and commenced treatment with calcium channel blockers, oral nitrates, statin
and ACE inhibitor.
Keywords: Diffuse coronary spasm, VT, STEMI
Since the CRP was normal we postulated that
transient myocardial ischaemia caused the
elevated WBC counts. His electrolytes including
Na, K and Mg were within normal limits. His 24
hour holter monitoring did not reveal much
abnormalities apart from few RVOT extra
systoles. His cardiac MRI did not reveal
significant abnormalities such as scarred
myocardium or left ventricular hypertrophy. Thus
the patient was diagnosed as vasospastic
myocardial infarction (MI) and discharged 2 days
later with calcium channel blockers (Diltiazem 30
mg bd) and oral nitrates. Patient was registered at
cardiology outpatient clinic for close follow up.
Discussion
Vasospastic angina is an important functional
cardiac disorder that leads to transient myocardial
ischemia and is caused by sudden, intense and
reversible coronary artery spasm resulting in
subtotal or total occlusion. Coronary vasospasms
may be focal or diffuse, and it can involve a single
or multiple epicardial coronary arteries. This
condition can present with spectrum of clinical
scenarios such as stable angina, acute coronary
syndromes and lethal arrhythmias. Vasospasm is
predominantly caused by hyper-reactive vascular
smooth muscle cells and probably endothelial
dysfunction which is not fully understood.
Prevalence of vasospastic angina has been
reported as low as less than 1% of hospital
admissions. Optimum administration of calcium
channel blockers is a promising therapeutic option
in preventing vasospastic angina and myocardial
infarctions.
Case report
A 64-year-old male patient with diabetes mellitus
and hypertension presented to our emergency
department with constricting type of chest pain
radiating to his back. He had nausea and sweating
too. The patient’s conscious level suddenly
deteriorated and he collapsed. Patient was attached
to a cardiac monitor and was found to have fast
ventricular tachycardia which evolved in to
ventricular fibrillation (Figure 1) with
haemodynamic instability. Patient was
resuscitated with DC cardioversion. His ECG
reverted back to sinus rhythm with ST segments
elevations were noted in V2 to V6 leads (Figure 2).
The patient was treated with loading doses of dual
antiplatelet agents (aspirin 300 mg and clopidogrel
600 mg PO), morphine sulphate 3 mg IV bolus and
5000 IU bolus of intravenous heparin. An urgent
2D echocardiogram was performed and it showed
ejection fraction of 55% with anterior and apical
wall hypokinesia. Coronary angiography (CAG)
was performed immediately. However, no critical
lesions were found. However, there was a 60%
discrete narrowing noted in mid circumflex artery
(Figure 2). In addition, another minor narrowing
was noted in proximal left anterior descending
artery. 100 micrograms of intra coronary
nitroglycerin (GTN) was administered and repeat
cineangiogram was performed. It showed
normalization of coronary arteries with no residual
stenosis (Figure 4). This was highly suggestive of
resolution of coronary artery spasms. Troponin-I
level of the patient was found to be 12.5 ng/L (0–
0.028). His full blood count was within normal
limits apart from neutrophil leukocytosis.
Ab
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Acute Anterior ST Elevation Myocardial
Infarction complicated with Ventricular
tachycardia due to Diffuse Coronary Artery
Spasms Wickramarachchi CP1, Senanayake S1, Lokuketagoda K1, Herath J 1,
Amarasena N1 Kottegoda S 1 1. Sri Jayewardenepura General Hospital, Sri Lanka.
Corresponding Author: Dr. C P Wickramarachchi
E-mail: [email protected]
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Sri Lankan Journal of Cardiology Volume 3: Issue 2 – June 2020
Figure 1: ECG: Ventricular tachycardia degenerates in
to ventricular fibrillation.
Figure 2: ST segment elevations in anterior precordial
leads
Figure 3: Significant narrowing at distal circumflex
artery.
Figure 4: Resolution of coronary artery spasms
following administration of intracoronary GTN.
Studies have shown that combination therapy of
statins with ACE inhibitors have beneficial effect
on vascular endothelial dysfunction, which also
aggravate coronary artery spasms.
References
1. Takagi Y, Takahashi J, Yasuda S, Miyata S, Tsunoda R, Ogata Y, et al. Prognostic stratification of patients with vasospastic angina:a comprehensive clinical risk score developed by the Japanese Coronary Spasm Association. J Am Coll Cardiol. 2013;62(13):1144–53. [PubMed]
2. Crea F, Lanza GA. New light on a forgotten disease:vasospastic angina. J Am Coll Cardiol. 2011;58(12):1238–40.
3. Kim MC, Ahn Y, Park KH, Sim DS, Yoon NS, Yoon HJ, et al. Clinical outcomes of low-dose aspirin administration in patients with variant angina pectoris. Int J Cardiol. 2013;167(5):2333–4.
4. Lanza GA, Careri G, Crea F. Mechanisms of coronary artery spasm. Circulation. 2011;124(16):1774–82.
5. The Task Force on the management of stable coronary artery disease of the European Society of Cardiology. 2013 ESC guidelines on the management of stable coronary artery disease—addenda. Eur Heart J. 2013;34(38):2949–30
6. Lanza GA, Sestito A, Sgueglia GA, Infusino F, Manolfi M, Crea F, et al. Current clinical features, diagnostic assessment and prognostic determinants of patients with variant angina. Int J Cardiol. 2007;118(1):41–7. [PubMed] [Google Scholar]
7. Lanza GA, Crea F. Pathophysiology and assessment of coronary spasm. In: Escaned J, Serruys PW, editors. Coronary Stenosis:Imaging, Structure and Physiology. New York, NY: Europa Editions; 2010. pp. 415–430.
8. Takagi Y, Yasuda S, Tsunoda R, Ogata Y, Seki A, Sumiyoshi T, et al. Clinical characteristics and long-term prognosis of vasospastic angina patients who survived out-of-hospital cardiac arrest:multicenter registry study of the Japanese Coronary Spasm Association. Circ Arrhythm Electrophysiol. 2011;4(3):295–302.
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Sri Lankan Journal of Cardiology Volume 3: Issue 2 – June 2020
A SION BLUE guide wire was used to cross the
LMCA to LAD lesions whilst a RINATO guide
wire was used to secure the left circumflex artery
(LCX). A 2.5 x 8mm NC HAWK balloon was used
to pre-dilate the LMCA to LAD lesions at pressure
of 6 to 8 atm. The LMCA to LAD was stented with
XIENCE EXPEDITION 3.0 x 38mm drug eluting
stent (DES), which was deployed at 10atm,
covering the ostium with minimum protrusion into
the aorta.
Figure 1:
Case report
A 61-year-old previously healthy lady was
investigated following a complaint of worsening
exercise tolerance since 1 month. She had a strong
family history of IHD and both of her siblings had
undergone PCI. There was no parental history of
IHD and both siblings were above the age of 50 at
the time of undergoing PCI. Her investigations
revealed lipid profile within normal range and there
was good glycemic control. Her electrocardiogram
(ECG) did not reveal any ischemic changes and
was in sinus rhythm. Her echocardiogram was
normal. Due to associated strong family history of
IHD, she underwent further investigation with
coronary angiography that revealed severe
atherosclerotic disease of the LMCA extending
into the LAD (Figure 1). She received initial
counselling to undergo CABG but opted for PCI
after refusal of CABG.
The PCI procedure was done with right side
femoral approach. A 7 Fr Judkins left (JL) catheter
was used to engage the left coronary system.
Catheter engagement and alignment was not
optimal throughout the procedure.
Ab
stra
ct
Distortion and Fracture of the proximal portion of a
stent in the left main coronary artery that was
successfully managed with a conservative
approach Boralessa MDS 1 , Sampath Withanawasam 1
1. Cardiology Unit, National Hospital Sri Lanka (NHSL), Colombo, Sri Lanka.
Corresponding author: Dr. M D S Boralessa
E-mail: [email protected]
Coronary stent distortion and fracture are rare and unfortunate events. It is associated with potential complications that include acute
coronary syndrome, stent thrombosis or in-stent restenosis that may require repeat revascularization of target vessels or even sudden
cardiac death. We present the case of a 61-year-old lady with a strong family history of ischemic heart disease (IHD), who was
evaluated for recent onset deteriorating exercise capacity. She underwent coronary angiography after preliminary investigations. The
angiography revealed severe atherosclerotic disease of her left main coronary artery (LMCA) extending into the left anterior
descending artery (LAD). The patient having refused cardiac bypass graft surgery (CABG) opted to proceed with percutaneous
coronary intervention (PCI) requiring stenting from the LMCA to LAD. Her PCI procedure was complicated with the development
of stent distortion followed by fracture of the proximal part of the LMCA stent. Procedure was stopped after kissing balloon dilatation
and Proximal Optimization Technique (POT) without implanting further stents. She remained clinically stable throughout the
procedure and was asymptomatic. She received close follow up and underwent a repeat check coronary angiography after 6 months
that revealed good angiography results with absence of in-stent restenosis or evidence of residual stent fracture. The patient clinically
improved and remained asymptomatic following PCI.
Key words: Left main coronary artery (LMCA), percutaneous coronary intervention (PCI), stent fracture
.
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Sri Lankan Journal of Cardiology Volume 3: Issue 2 – June 2020
The LMCA stent was post-dilated (POT) with
NC TREK 4.0 x 8 mm balloon at 18 - 24 atm. The
stent in the LAD was post-dilated with a 3.0 x
8.0 HAWK NC balloon at 16 - 24 atm and kept
in LAD for KBD. The LCx was rewired with the
existing RINATO guide wire to accomplish
KBD. 2.5 x 12 LACROSSE NC balloon was
unable to pass to LCx due to resistance at mid
LMCA. At this point, Stent visualization with
stent boost revealed severe distortion and fracture
of the proximal part of the LMCA stent, most
likely caused by attempted balloon advancement
on the LCX guidewire which traverse between
the wall of the LMCA and stent struts.
LMCA stent was re- dilated with 3.0 x 8.0 NC
balloon which was kept in LAD and then
repeated POT with 4.0x8.0 NC balloon. The
LCX was rewired and crossed with 1.5 x 8.0 SC
and 2.5 x 8.0 NC balloons sequentially. Kissing
balloon dilatation was performed with a
LACROSSE NC 2.5 x 10 mm balloon was placed
in the LAD and HAWK NC 2.5 x 8 mm balloon
in the LCX, whilst both balloons were inflated at
10 atm. A final POT was done with MOZEC NC
4.0 x 8mm balloon inflated at 20 atm. Stent
Boost revealed stent fracture with V shape gap
of the proximal portion of the LMCA stent
(Figure 2).
The patient remained clinically stable throughout
procedure. Despite the noted fracture, there was
TIMI III flow in the left system without evidence
of complications such as coronary dissection,
perforation or thrombus formation (Figure 3).
Figure 2:
Figure 2
Figure 3:
Thereafter, the next available options were
considered,
1. Deployment of an additional stent on the
proximal LMCA in order to superimpose the
fracture segment of the existing stent.
2. Conservative management – Observe and
intervene if the patient develops symptoms
or hemodynamic instability, in order to
reduce metal load that may occur with an
additional stent.
Since the patient was asymptomatic and
haemodynamically stable, a conservative
approach was decided. The patient’s recovery
period was uneventful and she was discharged
from the hospital 03 days after the procedure on
ticagrelor 90 mg/bd and aspirin 75 mg/ nocte
alone with other routine medicines. She
underwent close follow up. She was noted to
have improved exercise capacity following PCI.
She underwent a repeat check angiography 6
months later that revealed good angiography
results and absence of in-stent restenosis (Figure
4). Unfortunately, further detailed imaging of the
stent structure by intravascular ultrasound
(IVUS) or optical coherence topography (OCT)
could not be performed on this patient during
both times of angiography due to limited
resources and facilities available.
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Sri Lankan Journal of Cardiology Volume 3: Issue 2 – June 2020
Figure 4:
Discussion
Stent distortion (SD) is a rare event that can occur
even after successful deployment of a stent. It
may occur following several reasons due to
mechanical insults such as balloon dilatation over
a guidewire that traverses outside the stent
lumen, entrapment of guidewires, balloons or
other devices and balloon inflation of side
branches through the stent struts (1). There are
only few studies published regarding stent
distortion and awareness of the problem has only
recently emerged. Therefore further studies are
required to assess the magnitude and impact
associated with SD.
Stent fracture (SF) is defined as the loss of
continuity of the stent struts, as detected by
imaging modalities such as fluoroscopy, IVUS or
OCT (2). The detection of SF is important since it
may potentially cause stent thrombosis or
restenosis, which in turn may lead to acute
coronary syndrome (3). The incidence of
stent fracture (SF) ranges between 1 to 8% (4).
However, the incidence of SF may be
underestimated since it may be difficult to detect
SF with use of conventional angiography solely.
Several SF classification schemes have been
proposed based on the morphology of SF.
However a consensus is required for an accepted
universal classification.
A classification proposed by Nakazawa, et al (5),
classified SF into the following categories:
Grade I – Single strut fracture
Grade II – 2 or more struts fractured
Grade III – 2 or more struts fractured with
deformity
Grade IV – Complete transection of stent but
without a gap
Grade V – Complete transection causing a gap
in the stent
Among the many factors that predispose to
development of stent fracture,
1. Over expansion of the stent that may cause
weakening of stent struts (6)
2. Use of long length stents, that may undergo
higher radial force (6)
3. Overlapping of stents, that may cause
rigidity and create hinge points that can
deform the stent and lead to fracture (7)
4. Errors during handling of the stent (8)
5. Type of stenting technique e.g.; Crush
technique (9)
6. Anatomical factors such as angulated
vessels, tortuosity, long lesions, etc. (10).
The management of SF is dependent on many
factors such as the morphology of the fracture,
the presence of cardiac ischemia and the
presence of the above listed predisposing factors
of SF. However, further studies are required to
publish a consensus on the accepted
management of SF. The options of management
include conservative management, restenting or
surgical management (11).
Our patient’s PCI was complicated due to the
following reasons,
1. Poor guide catheter engagement that
provided poor support during the procedure
and caused technical difficulties during
rewiring of the LCX and passage of
balloons.
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Sri Lankan Journal of Cardiology Volume 3: Issue 2 – June 2020
2. The suspected passage of the guide wire
outside of the lumen of the stent in the
LMCA into the LCX, most likely caused by
inadequate deployment of the LMCA stent
due to lack of imaging modalities such as
IVUS and OCT to assess adequate stent
deployment.
3. Distortion of the stent during attempted
passage against resistance of the balloon into
the LCX on the guide wire.
4. Stent fracture caused by balloon passage
through the struts and dilatation of a distorted
stent at high pressures.
Despite the above complications the patient
remained stable during procedure and underwent
conservative management. The patient made an
uneventful recovery, she experienced
improvement of her symptoms and a repeat check
angiography demonstrated good results.
Conclusion This case highlights the importance of the need
of imaging modalities such as IVUS or OCT
during PCI to optimize stent deployment and
adequate apposition. This would prevent
complications such as inadvertent passage of
guidewires and devices outside of the stent lumen
and prevent consequences on the structure of the
stent. Therefore a high level of vigilance is
required if resistance is encountered during
rewiring and delivery of devices after
deployment of a stent. Adequate engagement of
guide catheters are essential, especially during
high risk PCI such as LMCA stenting in order to
reduce technical difficulties that may be
encountered during rewiring and delivery of
devices.
This case highlights that conservative
management without re-implanting a second
stent even at high risk sites like LMCA is
beneficial in selected patients despite presence of
stent fracture. Second stent implantation leaves
excess metal load in the vessel and is not hazard
free.
References
1. Hernandez RA, Surez A. Diagnosis and treatment of coronary stent entanglement complicated by extreme stent distortion. JIC, 3 March 2008; 30.
2. Lee SE, Jeong MH, Kim IS, Ko JS, Lee MG, Kang WY, et al. Clinical outcomes and optimal treatment for stent fracture after drug-eluting stent implantation. J Cardiol, 2009; 53: 422-428.
3. Shaikh F, Maddikunta R, Djelmami-Hani M, Solis J, Allaqaband S, Bajwa T. Stent fracture, an incidental finding or a significant marker of clinical in-stent restenosis? Catheter Cardiovasc Interv, 2008; 71: 614-618.
4. Alexopoulos D, Xanthopoulou I. Coronary Stent Fracture: How Frequent It Is? Does It Matter?. Hellenic J Cardiol, 2011; 52: 1-5.
5. Nakazawa G, et al. Incidence and predictors of drug-eluting stent fracture in human coronary artery a pathologic analysis. J Am Coll Cardiol, 2009 Nov 17; 54(21): 1924-1933.
6. Chhatriwalla AK, Unzek S, Kapadia SR. Recurrent Stent Fracture in the Right Coronary Artery. Clin Cardiol, 2010; 33: E70-2.
7. Leong DP, Dundon BK, Puri R, Yeend RA. Very late stent fracture associated with a sirolimus-eluting stent. Heart Lung Circ, 2008; 17: 426-428.
8. Ramegowda RT, Chikkaswamy SB, Bharatha A, Radhakrishna J, Krishnanaik GM, Nanjappa MC, et al. Circumferential Stent Fracture. Novel detection and treatment with the use of stent boost. Tex Heart Inst J, 2012; 39: 431-434.
9. Surmely JF, Kinoshita Y, Dash D, Matsubara T, Terashima M, Ehara M, et al. Stent strut Fracture –Induced restenosis in a bifurcation lesion treated with the crush stenting technique. Circ J, 2006; 70: 936-938.
10. Canan T, Lee MS. Drug-eluting stent fracture: Incidence, contributing factors, and clinical implications. Catheter Cardiovasc Interv, 2010; 75: 237-245.
11. Park KW, Park JJ, Chae IH, Seo JB, Yang HM, Lee HY, et al. Clinical Characteristics of Coronary Drug-Eluting Stent Fracture: Insights from a Two-Center DES Registry. J Korean Med Sci, 2011; 26: 53-58.
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Sri Lankan Journal of Cardiology Volume 3: Issue 2 – June 2020
Left anterior descending artery(LAD) lesion presenting as
acute inferior ST elevation myocardial infarction(STEMI) De Vas Goonewardane, APN 1; De Silva GID 2; Herath JH 2; Kottegoda, SR 2
1. Royal Brompton and Harefield NHS trust, UK.
2. Sri Jayawardenepura general hospital, Colombo, Sri Lanka.
Corresponding author: Dr De Vas Goonewardane.
E-mail: [email protected]
Inferior ST Elevation instead of reciprocal ST depression, along with a culprit LAD lesion is a rare combination. It is an important
association because of increased morbidity and mortality.69-year-old patient presented with subtle inferior ST elevation and ongoing
ischaemia. Catheterization revealed a culprit distal LAD lesion with a 90% plaque and high thrombus burden. Angioplasty and stenting
of the LAD restored TIMI 3 flow with pain resolution but failed to demonstrate a wrap-around path in RAO projection. Later he
developed V2-V5 ST elevation with symmetrical T wave inversion and concomitant worsening of inferior STE but was devoid of new
onset angina. Patient made an uneventful recovery to be discharged on day 5 of admission. Distal LAD occlusion, wrap-around LAD
path and previously ischaemic inferior territory with heavy collateral supply has been independently associated with concomitant inferior
STE during culprit LAD lesion. Careful scrutiny of angiogram and appropriate treatment is mandatory to improve acute and long term
outcomes.
Keywords: LAD lesion, Inferior STEMI
To our surprise culprit artery was found to be the
LAD with a 90% ulcerated plaque in mid-distal
vessel with high thrombus burden and distal TIMI
2 flow.
Right coronary (RCA) was dominant with minor
plaque involvement although the distal PLV and
PDA branches were small in calibre and diffusely
diseased. We proceeded with balloon angioplasty
and stenting of the LAD with a drug eluting stent
and intracoronary 2b/3A administration restoring
the TIMI 3 flow and alleviating the ischaemia.
Afterwards it was noticed that distal LAD was not
a wrap-a-round vessel which supplies a significant
area of the inferior myocardium in the right
oblique projection.
During post PCI stay in high dependency unit he
developed V2-V6 ST elevation followed by deep
symmetrical T wave inversions the following day
which is known to be a good prognostic sign in
terms of LAD revascularization(6).
Introduction
Inferior ST elevation instead of reciprocal ST
depression, along with a culprit LAD lesion is a
rare combination. This entity is important to
identify early because these patients have poor
outcomes with regards to morbidity and mortality (1,2). In most occasions the presentation is due to a
“wrap around apex” LAD which is one of the four
types of LAD distributions. But we present a case
of similar presentation without the so called
“wrap-around apex” path of LAD.
Case Report
69-year-old patient with diabetes mellitus
presented with acute ischaemic pain for two hours
duration. First EKG on admission revealed subtle
inferior ST elevation along with anteroseptal T
wave flattening. The findings were supported by
portable 2D Echo assessment showing inferior,
inferoseptal, anteroseptal hypokinesia with a
LVEF of 50%. Patient was taken immediately to
the cardiac catheterisation laboratory after initial
antiplatelet loading. Despite the ongoing
ischaemic pain his haemodynamic parameters
were stable with 130/70mmHg blood pressure and
a heart rate of 90/minute in sinus rhythm.
Ab
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A) ECG on admission prior to revascularization.
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Sri Lankan Journal of Cardiology Volume 3: Issue 2 – June 2020
In addition, the heart’s spatial placement in thorax,
Wilson’s central terminal placement, the presence
of previously silent-infarcted areas, asymmetric
distribution of the myocardial mass, or timing of
the ischemic process may all influence the
magnitude and the direction of the ischemic vector.
In our patient the explanation could be a
combination of above factors as well as
unidentified distal collaterals from LAD to inferior
segments which were clogged with thrombi during
the initial angiogram. Myocardial perfusion
imaging would be an objective way of assessing
ischaemic territory in these patients once stable.
References
1. Bozbeyoglu E, Yıldırımturk O, Aslanger E, Simsek B, Karabay CY, Ozveren O, et al. Is the inferior ST-segment elevation in anterior myocardial infarction reliable in prediction of wrap-around left anterior descending artery occlusion? Anatol J Cardiol 2019; 21: 253-8.
2. Kobayashi N, Maehara A, Mintz GS, Wolff SD, Généreux P, Xu K, et al. Usefulness of the Left Anterior Descending Artery Wrapping Around the Left Ventricular Apex to Predict Adverse Clinical Outcomes in Patients With Anterior Wall ST-Segment Elevation Myocardial Infarction (an INFUSE-AMI Substudy). Am J Cardiol 2015; 115: 1389-95.
3. Sunil Roy TN, Nagham JS, Kumar RA. Acute inferior wall myocardial infarction due to occlusion of the wrapped left anterior descending coronary artery. Case Reports in Cardiology. 2013. Article ID: 983943, 3 pages. http://dx.doi. org/10.1155/2013/983943.
4. Lew AS, Hod H, Cercek B, Shah PK, Ganz W. Inferior ST segment changes during acute anterior myocardial infarction: a marker of the presence or absence of concomitant inferior wall ischemia. J Am Coll Cardiol 1987; 10: 519-26.
5. Hossein S, Kheirieh A, Azmoodeh E. Inferior ST-Segment Elevation Caused by Occlusion of Left Anterior Descending Artery. Journal of Medicine and Life Vol. 13, Issue 1, January-March 2020, pp. 98–101
6. Lee MJ, Jang JH et al. Prognostic Implications of Newly Developed T-Wave Inversion after Primary Percutaneous Coronary Intervention in Patients with ST-Segment Elevation Myocardial Infarction. Am J Cardiol. 2017;119 (4):515-519.
Baseline investigations revealed haemoglobin of
13.2g/dl, Platelet of 188000/ul, Troponin I titre of
37.16 ng/ml and serum creatinine of 104 umol/l.
Repeat ECHO assessment showed resolution of
previously noted anteroseptal hypokinesia and
patient made an uneventful recovery to be
discharged on day 5 of admission. ECHO
assessment showed resolution of septal
hypokinesia but persistent mild inferior segmental
defects.
Discussion
The inferior lead (ii, iii, aVF) ST elevation is
traditionally associated with either a RCA or a
dominant circumflex lesion. Very rarely one can
encounter a wrap-a-round LAD which supplies at
least one fourth of inferior segments in right
oblique projections of the heart (3). It was unique in
this case that initially inferior changes were not
associated with prominent anterior EKG changes
though the lesion was in mid to distal LAD. In
addition, our patient did have a mid-distal LAD
occlusion without being wrap- around which is
rarer (1). On the other hand, distal LAD lesions may
cause inferior STE without inferior wall
involvement due to the injury vector being directed
left and downwards. Attenuation of the usually
expected reciprocal ST depression in inferior ECG
leads is also an indirect clue to dominant LAD
supply in some patients (4). Features put forward in
previous studies for concomitant/isolated inferior
STE in LAD occlusion are (5),
1. The site of LAD artery occlusion (distal
occlusion).
2. LAD artery extension on the inferior wall of
left ventricle (wrap-around LAD)
3. Collateral flow from the LAD artery to the
inferior wall.
The LAD artery holds added importance in all of
these patients and careful scrutiny of the angiogram
is necessary to pick the culprit lesion.
Ischemic myocardium subtended by the infarct-
related artery may not exhibit a uniform degree of
ischemia due to a heterogenous collateral network.
B) ECG on Day 1 post Revascularization.
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Retrieval of a stalled rotablator burr using a modified
double guide-guideliner technique Kabir T1 , Panoulas V1 , De Vas Goonewardane APN 1
1. Royal Brompton and Harefield NHS trust, UK.
Corresponding author: Dr De Vas Goonawardana.
E-mail: [email protected]
Lesion modification through Rotablation is well-established and extensively practiced worldwide. It demands certain amount of
technical expertise to master. Out of the possible complications stalled burr is a dreaded and life-threatening complication. An 83-year-
old male was referred on emergency basis with a stalled rotablation burr in LAD (Left anterior descending). He was ischaemic and
maintaining a marginal blood pressure on an intra-aortic balloon pump and fluids. Surgical options were limited and decision was made
to attempt a high-risk retrieval. 8Fr Parallel guide was placed via the left femoral artery. Multiple parallel wires used to cross the burr
position were in vain. Limited small balloon inflations were performed in the region of interest. 7 French Guideliner over the cut rota
burr was not successful either. Burr was finally retrieved using NC balloon to trap Rota stem within the Guideliner at high pressures.
Procedure was completed with implantation of two stents to LAD after further rotablation. IVUS (Intra-vascular ultrasound) run
confirmed satisfactory results. Most complications of Rotablation is due to technical deficiencies. It is very important to get extensively
trained under an experienced operator in terms of the technique and bailout strategies during complications. Every situation is unique
and demands a custom-tailored approach. Here we propose a technique of retrieval, combining double wire and guide liner techniques.
Keywords: Rotablation, IVUS, LAD, stalled burr, retrieval
Ultimately the burr was retrieved with gentle
traction along with a 2.5x30-NC balloon trapping
the burr stem within the guideliner and guide
catheter at high pressure of 30ATM. This then
enabled PCI to the LAD and left main stem to be
undertaken sequentially using the left femoral
guide system which was already in place.
Procedure was completed with implantation of two
stents after further rotablation with TIMI 3
antegrade flow (Figure 3). IVUS (Intra-vascular
ultrasound) run was carried out to exclude
complications and confirm adequate stent
expansion.
Case Report We report a case of an 83-year-old male
undergoing angioplasty following admission with
a troponin positive acute coronary event to a
district general hospital. After initial diagnostic
views through radial access it was planned to
perform upfront rotablation in view of lesion
modification. Unfortunately during this procedure
the 1.5mm rotablation burr stalled and was not
retrievable (Figure 1). After trying all the
possibilities locally, the symptomatic patient was
rushed to our center by paramedics with an intra-
aortic balloon pump inserted from right femoral
artery.
Immediate surgical opinion was sought and
surgeons decided that it was not likely to yield a
positive outcome unless as a bailout strategy.
First a parallel guide was placed via the left
femoral artery using an 8 French sheath. An 8
French EBU 3.5 guide catheter was co-aligned.
Heparin was administered keeping the ACT at a
higher range between 300-350. Using a variety of
parallel wires including Sion Black, Whisper and
Fielder XT attempts to loosen up the plaque was
carried out using a 1.0, 1.5 and 2.0 balloons. But it
was not possible to negotiate any wire beyond the
stalled burr.
An attempt was made to retrieve the 1.5mm rota
burr with a 7 French guideliner over the cut rota
burr (Figure 2) through radial guide which was not
successful. During the procedure there was a
transient cardiac arrest which responded to CPR
and adrenaline injection.
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Figure1- Stalled LAD burr with intra-aortic
balloon on background.
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We describe a modified technique by combining
few of these techniques including disassembly of
rotor driveshaft. We conclude that meticulous
attention to the technique should be adhered to
during rotablation at all times and that necessary
hardware and human expertise to be in vicinity
should a need arise for treating a rotablation
complication.
References 1. Mechery A, Jordan PJ, Doshi SN, Khan SQ. Retrieval of
a stuck Rotablator burr ("Kokeshi phenomenon") and successful percutaneous coronary intervention. J Cardiol Cases. 2015;13(3):90‐92. Published 2015 Dec 10. doi:10.1016/j.jccase.2015.10.012
2. Chiang CH, Liu SC. Successful Retrieval of an Entrapped Rotablator Burr by Using a Guideliner Guiding Catheter and a Snare. Acta Cardiol Sin. 2017;33(1):96‐98. doi:10.6515/acs20160404a
3. Kimura M, Shiraishi J, Kohno Y. Successful retrieval of an entrapped Rotablator burr using 5 Fr guiding catheter. Catheter Cardiovasc Interv. 2011;78(4):558‐564. doi:10.1002/ccd.22995
Figure 2- Parallel guide technique of wiring pass the
burr.
Figure 3- Final cineangiogram after stent placement.
Discussion
This entrapment of a rota burr is a rare phenomenon,
associated with significant anxiety and usually
demanding for surgical measures. The Japanese have
termed this the “Kokeshi phenomenon” named after a
wooden doll found in northern Japan1.
There are several bailout endovascular approaches
that have been proposed, including simple manual
traction, deep engagement, parallel guide wire and
balloon inflation to loosen, using a snare for forceful
local traction, or a child-in-mother catheter to
facilitate the successful retrieval2,3.
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On examination she had absent dorsalis pedis,
popliteal and posterior tibial artery pulsation with
ABI of 0.6. Left foot ulcer noted without
granulation tissue. Bilateral lower limb arterial
duplex revealed severe occlusive arterial disease at
both fem-pop regions.
Peripheral Intervention
Via right femoral retrograde puncture (6FG), left
leg angiography was performed, which identified
a distal popliteal chronic total occlusion (CTO)
with bridging collaterals (Image 1).
Image 1 - Distal popliteal artery CTO with bridging
collaterals
Left femoral artery anterograde access was gained
via 6FG vascular sheath and CTO site engaged
with Judkin Right (JR) 3 guide catheter. CTO was
crossed with Fielder XT (0.014”) coronary guide
wire with FineCross micro-catheter support. Wire
exchanged to Asahi Sion guidewire (0.014”).
Lesion predilated with Sapphire 2.5x12 mm
normal pressure balloon at 8 atm (Image 2).
Introduction
Endovascular interventions for PAD mainly
focused on the descending aorta, iliac, femoral and
popliteal arteries. Peripheral vascular intervention
(PVI) offers a much lower periprocedural risk.
This prevents major amputation of a limb which is
associated with loss of independence, diminished
quality of life, and poor overall survival. Critical
limb ischemia defined as presence of ischemic rest
pain, ulceration, or gangrene caused by critically
diminished perfusion attributable to occlusive
arterial disease and is usually associated with an
Ankle-Brachial Index (ABI) <0.4 and toe pressure
<30 mm Hg (Rutherford–Baker stages 4–6 and
Fontaine stages III and IV). Intermittent
claudication (IC) typically presents as leg
cramping with exercise that is relieved by rest. The
claudication distance gradually decreases with
progression of the disease. Femoro-popliteal
(Fem-Pop) region is the longest artery with fewest
side branches, and the most common location of
occlusive disease precipitating IC. Self-expanding
stents, drug eluting stents and drug coated balloon
(DCB) angioplasty are the mainstay of treatment
strategies in managing fem-pop lesions.
Case History
62 years old female with diabetes mellitus for 15
years duration had IC of 6 months duration. She
had undergone amputation of four lateral toes and
developed a non-healing ulcer at the surgical
incision, which had poorly responded to both
medical and surgical adjunct therapies. She was
determined to be in Rutherford–Baker stage 5 with
ischemic ulceration limited to digits. She had no
other clinically significant occlusive arterial
diseases elsewhere and diabetes was controlled
(HbA1C- 7.5%) with insulin therapy.
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A case of Peripheral Vascular Intervention for
Chronic Total Occlusion of the Popliteal Artery
D.M. Liyanage1, N. Fernando1, T. Vaikunthan1, L.S. Kularatne1
T. Pereira1
1. Institute of Cardiology, National Hospital of Sri Lanka.
Corresponding Author: Dr D M Liyanage. E Mail: [email protected]
Peripheral arterial disease (PAD) consists of a spectrum from asymptomatic stenosis to limb-threatening ischemia. During the last
decade a tremendous number in the variety of endovascular devices and techniques available to treat occlusive disease have emerged
and this has resulted in a shift from open surgical revascularization to percutaneous endovascular therapy as a first option. We report a
62 years old female patient with diabetes mellitus with poorly healing left lower limb wound and a history of intermittent claudication
in both lower limbs, who had chronic total occlusion of the left popliteal artery which was opened employing a drug eluting stent (DES)
and drug coated balloon (DCB).
Keywords: Peripheral arterial disease, Peripheral vascular interventions, Critical limb ischemia, chronic total occlusion
.
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Proximal popliteal artery over the knee joint area
was treated with In.Pact Falcon Paclitaxel coated
balloon at 8 atm (Image 3).
CTO segment stented with Xience Prime 2.75x38
mm Everolimus eluting stent at 10 atm (Image 4).
Post procedure angiogram revealed excellent
results with brisk 3 vessel run off (Image 5)
Patient made an uneventful recovery and ABI fell
to 0.8 at 24 hours. Her lower limb wound
completely healed 4 weeks after post procedure
(Image 6) and she remains asymptomatic at 6
months.
Image 2 – Pre-dilatation of CTO segment
Image 3 – Proximal popliteal artery dilatation with
Paclitaxel eluting balloon
Image 4 – CTO segment stenting with Everolimus
eluting coronary stent (2.75x33 mm)
Image 5- Final angiogram with good distal run off
Image 6- Healed surgical site wound one month after
procedure
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Discussion Endovascular therapy is now established to treat
lower-extremity peripheral arterial diseases
including CTO (1), as an alternative to surgical
revascularization (2). Even though patients are
benefitted by low perioperative risk and less
hospital stay compared to surgical interventions (3,4,) a number of procedural complications as well
as long term complications have been described
with PVI. Arterial dissection, perforations,
vascular access haematoma formation are seen
immediately and re-stenosis, stent fracture and
dislocation are seen later. Popliteal artery is an
area of high mechanical stress and dynamic force
which has been associated with accelerated
restenosis and high rates of stent fracture and
occlusion. Although newer stents improved
outcomes in this territory, in-stent restenosis is
still recognized as a challenging complication in
patients with PAD (5). Use of DES over bare
metal stents has shown superior outcome with
higher patency rate (6). DCB potentially benefit
by avoiding stenting where there is a high risk of
stent fracture, occlusion and long term dual anti
platelets. Re-stenosis rates were lower in DCB
over plain balloon angioplasty (7,8). In our patient,
advance precautions which we have taken led to
an uncomplicated procedure. The strategy which
we have employed in this patient by avoiding
stenting at the knee joint and use of DCB instead
will lead to long term patency rate. Post
procedural care and surveillance should target the
durability of the endovascular procedure with a
multi-disciplinary approach. Promotion of
regular exercise, control of vascular risk factors,
continuation of drug treatment, periodic
assessment of vessel patency and timely re-
intervention are vital in the post-operative
management. In our patient dual anti-platelet
therapy was advised for one year followed by
aspirin alone lifelong with continuous
surveillance.
References 1. K.A. Gallagher,A.J. Meltzer, R.A. Ravin, A. Graham,
G.Shrikhande, P.H. Connolly, et al.Endovascular management as first therapy for chronic total occlusion of the lower extremity arteries: comparison of balloon angioplasty, stenting, and directional atherectomyJ Endovasc Ther, 18 (2011), pp. 624-637
2. Rowe VL, Lee W, Weaver FA, Etzioni D. Patterns of treatment for peripheral arterial disease in the United States: 1996-2005.J Vasc Surg. 2009; 49:910–91
3. A.W. Bradbury, D.J. Adam, J. Bell, J.F. Forbes, F.G.Fowkes, I. Gillespie, et al., BASIL trial ParticipantsBypass versus Angioplasty in Severe Ischaemia of the Leg (BASIL) trial: An intention-to-treat analysis of amputation-free and overall survival in patients randomized to a bypass surgery-first or a balloon angioplasty-first revas- cularization strategy J Vasc Surg, 51 (5 Suppl) (2010), pp. 5-17S
4. N.N. Egorova, S. Guillerme, A. Gelijns, N. Morrissey, R. Dayal, J.F. McKinsey, et al.An analysis of the outcomes of a decade of experience with lower extremity revascularization including limb salvage, lengths of stay, and safety J Vasc Surg, 51 (2010), pp. 878-885 885.e1
5. Parthipun A, Diamantopoulos A, Kitrou P, et al. Use of a new hybrid heparin-bonded nitinol ring stent in the popliteal artery: procedural and mid-term clinical and anatomical outcomes. Cardiovasc Intervent Radiol. 2015;38:846-854
6. De Cock E, Sapoval M, Julia P, de Lissovoy G, Lopes S.A budget impact model for paclitaxel-eluting stent in femoropopliteal disease in France. Cardiovasc Intervent Radiol. 2013; 36:362–370. doi: 10.1007/s00270-012-0494-x.
7. Tepe G, Zeller T, Albrecht T, Heller S, Schwarzwälder U, Beregi JP, Claussen CD, Oldenburg A, Scheller B, Speck U.Local delivery of paclitaxel to inhibit restenosis during angioplasty of the leg.N Engl J Med. 2008; 358:689–699. doi: 10.1056/NEJMoa 0706356.
8. Werk M, Albrecht T, Meyer DR, Ahmed MN, Behne A, Dietz U, Eschenbach G, Hartmann H, Lange C, Schnorr B, Stiepani H, Zoccai GB, Hänninen EL.Paclitaxel-coated balloons reduce restenosis after femoro-popliteal angioplasty: evidence from the randomized PACIFIER trial.Circ Cardiovasc Interv. 2012; 5:831–840. doi: 10.1161/CIRCINTE-RVENTIONS.112.971630.
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Her echocardiogram showed good systolic and
diastolic functions without any wall motion
abnormality while troponin I was rising from 1.4
to 8.6 ng/mL. An emergency coronary angiogram
was performed which showed a spontaneous Left
Anterior Descending Coronary Artery (LAD)
dissection with a TIMI III distal flow (Figure 1a).
The rest of the coronary circulation was normal. It
was decided to manage the patient medically and
she was discharged after a course of LMWH once
the ischemic chest pain completely resolved with
minimal ECG changes.
One week later, the patient was complaining of
class III angina and was readmitted for further
evaluation and management. An urgent repeat
angiography showed the same proximal to mid
vessel dissection of the LAD. An intravascular
ultrasound scan (IVUS) was performed over the
dissected segment of LAD. The dissection flap of
29mm in length proximal to D1 was visualized
(Figure 1b). An ostial to proximal LAD stenting
with a Drug Eluting Stent was done. The post
stenting IVUS showed optimal stent deployment
and the post stenting angiography revealed TIMI
III flow in LAD and all its’ branches.
The patient had a significant improvement of her
symptoms soon after the procedure and she was
free of angina on discharge. The patient was kept
on a beta blocker with DAPT and referred to a
gynecologist for a permanent method of
contraception after explaining the high risk for
pregnancy.
Introduction Non-atherosclerotic Spontaneous Coronary Artery
Dissection (NASCAD) is the term used to indicate
a non-traumatic and non-iatrogenic separation of
the coronary arterial wall possibly due to either an
intimal tear or a bleeding of vasa vasorum,
resulting in an intra-medial hemorrhage. In
contrast to atherosclerotic SCAD which is limited
in extent by medial atrophy and scarring,
NASCAD can involve extensive lengths. SCAD is
a rare cause for acute coronary syndrome (ACS)
with a reported incidence of 0.1-4 % of cases in the
general population (1). Nearly a quarter of ACS in
women less than fifty years are noted to be due
to SCAD. The possible predisposing factors
identified for NASCAD are post-partum status,
fibro-muscular dysplasia (FMD), hormonal
therapy, multiparity (>4 births), systemic
inflammatory conditions and connective tissue
disorders (2).
Case Presentation A 27-year-old mother of two who was previously
well, had presented to the local hospital with acute
ischemic chest pain of one day duration. She was
diagnosed to have Non-ST Elevation Myocardial
Infarction (NSTEMI) with inferior territory
involvement. She was transferred to the Institute
of Cardiology, National Hospital of Sri Lanka
(NHSL) for further management.
On presentation to NHSL, patient was
complaining of persistent chest pain and ECG
showed sinus bradycardia with biphasic T in leads
aVL, II, III and aVF.
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A 27-year-old Lady with Non-atherosclerotic
Spontaneous Left Anterior Descending
Coronary Artery Dissection
Prabath IHDS 1, Fernando N 1 , Pereira T1
1. Institute of Cardiology, National Hospital of Sri Lanka.
Corresponding Author: Dr. I.H.D.S. Prabath Email: [email protected]
We report a young lady who presented with non-atherosclerotic spontaneous LAD coronary artery dissection who was managed with
percutaneous coronary intervention after failed conservative approach. The utility of intravascular ultrasound technology in diagnosis,
management and the technically difficult nature of interventional approach in arterial dissection are highlighted.
Keywords: Non-atherosclerotic coronary artery dissection, Coronary dissection
.
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Discussion
NASCAD mainly manifests with typical
characteristic symptoms and signs of myocardial
infarction which yet can have diverse
presentations. The most frequently affected
vessel is LAD (3). The corner stone of the
diagnosis of NASCAD is the coronary
angiography. A high degree of suspicion is
needed in the proper context to plan for further
evaluation with optical coherence tomography
(OCT) or IVUS. Alternatively, the coronary
angiography could be repeated in 4-6 weeks to
detect the spontaneous healing of the dissected
segment.
If the patient is clinically stable with a non-
critical luminal obstruction and a TIMI III distal
flow, conservative approach is recommended in
most spontaneous SCAD. However, patients
presenting with ACS with ongoing symptoms of
ischemia and/or haemodynamic compromise
must be considered for revascularization (4).
In this case, we undertook latter approach even
though the PCI is technically challenging
associated with higher complication rates and
failure in SCAD. The patients with SCAD will
benefit from long term DAPT, a beta blocker and
a statin if dyslipidemia is present. A reduced
recurrence of SACD is observed with the usage
of a beta blocker (5).
Conclusion
A high index of suspicion is important in the
diagnosis of NASCAD, where a conservative
approach is preferred over revascularization
strategy when appropriate.
References
1. Hayes SN, Kim ESH, Saw J, et al. Spontaneous Coronary Artery Dissection: Current State of the Science: A Scientific Statement from the American Heart Association. Circulation, 2018; 137: e523.
2. Saw J, Aymong E, Sedlak T, et al. Spontaneous coronary artery dissection: association with predisposing arteriopathies and precipitating stressors and cardiovascular outcomes. Circ Cardiovasc Interv, 2014; 7:645.
3. Tweet MS, Hayes SN, Pitta SR, et al. Clinical features, management, and prognosis of spontaneous coronary artery dissection. Circulation, 2012; 126: 579.
4. Hayes SN, Kim ESH, Saw J, et al. Spontaneous Coronary Artery Dissection: Current State of the Science: A Scientific Statement from the American Heart Association. Circulation, 2018; 137: e523.
5. Saw J, Humphries K, Aymong E, et al. Spontaneous Coronary Artery Dissection: Clinical Outcomes and Risk of Recurrence. J Am Coll Cardiol, 2017; 70: 1148.
b
)
a
)
Figure 1- (a) Left Anterior Descending Coronary Artery (LAD) dissection with a TIMI III distal flow
(b) The dissection flap of 29mm in length proximal to D1
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The physical examination revealed peripheral
edema, gross ascites and elevated jugular venus
pressure. The precordial examination revealed a
normal heart size and diminished heart sounds with
a pericardial knock. Routine blood examination
including full blood count (FBC) and liver function
test results were normal with normal inflammatory
markers. An electrocardiogram showed a normal
sinus rhythm with a heart rate of 90 beats/min. Two
dimensional echocardiography (2D Echo) revealed
severe calcification of both parietal and visceral
pericardium with thin pericardial effusion and
preserved left ventricular ejection fraction (EF).
Both left and right atria were dilated with plethoric
inferior vena cava. Doppler study showed
constrictive physiology of the mitral valve with
increased E-wave velocity and shortened
deceleration time with a small A-wave. Tissue
Doppler image revealed preserved early diastolic
mitral annular velocity (e') with the ratio between
lateral and septal mitral annulus as well as tricuspid
annulus being significantly reduced.
The chest radiograph (CXR) revealed diffuse and
dense calcification of the pericardium without
evidence of old or active tuberculosis. A thoracic
computed tomographic (CT) scan demonstrated a
calcific pericardium surrounding the entire heart
involving both parietal and visceral pericardium.
Introduction
Constrictive pericarditis (CP) is a relatively
uncommon entity leading to clinical heart failure,
which is characterized by an inflammatory process
that leads to progressive fibrous thickening or/ and
calcification of the pericardium resulting in
pericardial non-compliance. The presence of
pericardial calcification is a cardinal feature of CP,
However the absence of it does not exclude the
diagnosis (1). The most common identifiable cause
of CP are tuberculosis, previous open heart surgery
and mediastinal irradiation (2). Other possible
causes include connective tissue diseases,
malignancy, chronic renal failure, trauma and
infections (1). However, more than half of cases are
idiopathic with no identifiable cause found (1).
The diagnosis of constrictive pericarditis has been
challenging even though multiple diagnostic
modalities have been developed. However, because
it is potentially reversible, the diagnosis must not be
missed. Surgical pericardiectomy has the ability to
cure CP, with dramatic improvements in symptoms
and quality of life (2, 3).
Case report
A 32-year-old previously healthy male presented
with fatigue, gradually worsening dyspnea on
exertion, abdominal distention and pedal edema for
more than one year duration. There was no history
of fever or cough.
Idiopathic Calcific Constrictive Pericarditis,
successfully treated with Surgical
Pericardiectomy
N.U.A. Dissanayake1, Gamini Galappatthy1, A.K Pathirana1, Rajitha Y De
Silva2, C.I.H. Siriwardane1, I.U.K. Marasinghe1
1 Institute of Cardiology, National Hospital of Sri Lanka.
2 Cardio thoracic unit, Sri Jayawardhanapura General Hospital,
Corresponding author: Dr. N.U.A. Dissanayake
E-mail: [email protected]
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Constrictive pericarditis is a potentially curable condition caused by different aetiologies. It is an uncommon entity in clinical
practice and challenging to diagnose. Therefore, a high degree of clinical suspicion and use of multimodality imaging approach
is required to achieve a diagnosis. Herein, we present a case of idiopathic calcific constrictive pericarditis, which was diagnosed
with the help of multimodality imaging approaches such as two dimensional echocardiography and computed tomographic
scan. The patient presented with features of right heart failure. There was failure of response to initial medical therapy with
diuretics, however his symptoms improved dramatically after surgical pericardiectomy. This case demonstrate the classic
presentation of constrictive pericarditis, investigation required and their findings to diagnose, and provides a discussion of the
benefit and outcomes of prompt treatment.
Key words: Constrictive pericarditis, Constrictive physiology, Mitral annular motion, Pericardiectomy, Right heart failure.
.
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Figure 1: Chest X-ray lateral and PA views – Pericardial calcification
Figure 2: CT chest – Pericardial calcification
Figure 3: Before and after the surgical pericardiectomy
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The consent for surgery was given by the patient
due to continued deterioration of his clinical
condition with features of severe right heart
failure leading to poor quality of life while on
medical management. Successful surgical
pericardiectomy was done without major
complications and patient had dramatic
improvement of his symptoms and quality of life.
Discussion
Constrictive pericarditis is a condition, which
leads to decreased compliance of the pericardium
due to pericardial thickening and fibrosis with or
without calcification. This may result in impaired
ventricular diastolic filling and right heart
failure(1). The most common causes of
constrictive pericarditis are idiopathic and
followed by previous cardiac surgery and
mediastinal irradiation(2). Tuberculous peri-
carditis is an important aetiology in developing
countries.
The symptoms of CP develop slowly over a
number of years and there are no clinical features
specific to CP. The classical presentation of
constrictive pericarditis is similar to symptoms
and signs of chronic right heart failure (RHF).
Fatigue, dyspnea on exertion, orthopnea, lower
leg oedema, hepatic congestion with subsequent
development of ascites, abdominal discomfort,
anasarca, and jaundice are the common clinical
manifestation of CP. However, other cardiac and
non cardiac diseases can present with similar
symptoms, specially restrictive cardiomyopathy
and tricuspid valve dysfunction can cause signs
and symptoms of right heart failure similar to CP (4). Therefore high degree of clinical suspicion(5)
and multimodality imaging approach(1) is needed
to evaluate a patient with symptoms of RHF to
diagnose CP.
Echocardiography would be considered as the
first-line diagnostic modality and constrictive
pericarditis should be suspected in patients
presenting with heart failure symptoms and
preserved ejection fraction as in our patient. Respiration-related ventricular septal shift,
restrictive mitral inflow velocity (E/A ratio > 0.8),
preserved or accelerated medial mitral annular
motion (e’velocity > 9cm/sec), reversal of the
relationship between lateral to medial annular
tissue Doppler velocities (also called annulus
reversus).
Hepatic vein expiratory diastolic reversal and
plethoric inferior vena cava (6,7) should alert the
interpreting clinician to the diagnosis of CP.
Although these Doppler findings are usually
diagnostic, both false-positive and false-negative
results exist. Therefore single echocardiographic
parameter should not be used exclusively to
diagnose CP rather than multifaceted approach.
Even though echocardiography is not considered
as a reliable technique to visualize the
pericardium, CT and magnetic resonance (MR)
imaging can directly demonstrate the morphology
of pericardium. Therefore CT and MRI are
recommended in the assessment of pericardial
morphology in CP, which revealed generalized
pericardial thickening and pericardial
calcifications (1). In patients with appropriate
clinical manifestations, pericardial thickness of
>5 to 6 mm is highly specific and >4 mm is
suggestive of pericardial constriction (1). But the
absence of pericardial thickening does not
exclude the diagnosis, because up to 20% of
patients with surgically confirmed constrictive
pericarditis showed normal pericardial thickness
on imaging studies (5).
Pericardial calcifications are an important finding
in imaging study, which is highly suggestive of
constrictive pericarditis (8), regardless of the
degree of pericardial thickening.
Our patient presented with classic symptoms and
signs of right heart failure and the transthoracic
echocardiogram revealed right heart failure with
constrictive physiology of the mitral and tricuspid
valves. A chest radiograph showed pericardial
calcification, and the chest CT confirmed the
diagnosis with pericardial thickening and
calcification.
The primary goal in management of CP is to
improve cardiac function, haemodynamic and
symptoms. It is crucial to identify the primary
aetiology and be managed accordingly. The
definitive treatment for CP is complete surgical
pericardiectomy and should be carried out
whenever feasible (9).
Pericardiectomy generally cure the CP with rapid
haemodynamic and symptomatic improvements
in most patients.
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At present, with improved technique and skill,
pericardiectomy is generally a safe procedure,
although the early post-operative death risk is
more than 2%. Survival rates vary from 55% to
90% on the basis of age, sex, and race (10).
Even though medical management of CP remains
controversial, careful observation and
symptomatic treatment, has been suggested in less
severe cases. A strict fluid restriction, low sodium
diet and diuretics have been used in the early
stages of the disease to improve pulmonary and
systemic congestion. However, diuretics should
be used cautiously as any drop in intravascular
volume may lead to a significant drop in cardiac
output.
Medical management was unsuccessful in our
patient. A medically treatable aeitiology could not
be identified despite extensive investigations.
Therefore, the best option for the management of
our patient was complete surgical
pericardiectomy in view of complete cure.
Conclusion
The diagnosis of constrictive pericarditis is still
challenging. High degree of clinical suspicion,
multimodality imaging approach including
echocardiogram, chest radiography, CT and MRI
are needed for more accurate diagnosis and to
decide the optimal treatment option for patients
with constrictive pericarditis. When there is no
medically treatable aetiology, surgical peri-
cardiectomy is the best treatment option which
can cure CP.
References
1. Bogaert J, Francone M. Pericardial disease: value of CT and MR imaging. Radiology, 2013; 267:340-356. doi: 10.1148/radiol.13121059. [PubMed] [CrossRef]
2. Ling LH, Oh JK, Schaff HV, Danielson GK, Mahoney DW, Seward JB, Tajik AJ. Constrictive pericarditis in the modern era: evolving clinical spectrum and impact on outcome after pericardiec-tomy. Circulation, 1999; 100: 1380-1386. doi: 10.1161/01.CIR.100.13.1380. [PubMed] [CrossRef]
3. Geske JB, Anavekar NS, Nishimura RA, Oh JK, Gersh BJ. Differentiation of constriction and restriction: complex cardiovascular hemodynamics. J Am Coll Cardiol, 2016; 68: 2329-47.
Conclusion
DLVOT is not an infrequent phenomenon.
Identifying patient and procedure risk factors
that possibly unmask DLVOT will help identify
potential candidates who may elicit DLVOT.
Regardless managing DLVOT can be both
confusing and challenging to an otherwise non-
suspecting team and can result in morbidity and
mortality if not recognized in a timely manner.
Contrary to normal wisdom prompt hydration
and beta blockers can be lifesaving. Considering
TAVR still remains an expensive modality of
therapy in moderate to high risk patients, greater
consideration should go into the potential of post
procedure complications like DLVOT which
may adversely affect outcome. Thus stressing the
need for better patient selection, overall
vigilance and early anticipation an action when
DLVOT occurs.
References
1. Sobczyk D. Dynamic left ventricular
outflow tract obstruction: underestimated
cause of hypotension and hemodynamic
instability. Journal of Ultrasonography,
2014; 14(59):421-7.
2. Panduranga P, Maddali MM, Mukhaini MK,
Valliattu J. Dynamic left ventricular outflow
tract obstruction complicating aortic valve
replacement: A hidden malefactor revisited.
Saudi Journal of Anaesthesia, 2010; 4(2):
99-101.
3. Makhija N, Magoon R, Balakrishnan I, Das
S, Malik V, Gharde P. Left ventricular
outflow tract obstruction following aortic
valve replacement: A review of risk factors,
mechanism, and management. Annals of
Cardiac Anaesthesia, 2019; 22(1): 1-5.
4. Bergman M, Vitrai J, Salman H. Constrictive pericarditis: a reminder of a not so rare disease. EurJ Intern Med, 2006; 17: 457-464. doi: 10.1016/j.ejim. 2006.07.006. [PubMed] [CrossRef]
5. Nishimura RA. Constrictive pericarditis in the modern era: a diagnostic dilemma. Heart, 2001; 86: 619-623. doi:10.1136/heart.86.6.619. [PMC free article] [PubMed] [CrossRef]
6. Oh JK, Tajik AJ, Appleton CP, Hatle LK, Nishimura RA, Seward JB. Preload reduction to unmask the characteristic Doppler features of constrictive pericarditis: a new observation. Circulation, 1997; 95: 796-9.
7. Reuss CS, Wilansky SM, Lester SJ, et al. Using mitral ‘annulus reversus’ to diagnose constrictive pericarditis. Eur J Echocardiogr, 2009; 10: 372-5.
8. Isner JM, Carter BL, Bankoff MS, Konstam MA, Salem DN. Computed tomography in the diagnosis of pericardial heart disease. Ann Intern Med, 1982; 97: 473-479. doi: 10.7326/0003-4819-97-4-473. [PubMed] [CrossRef]
9. Glenn F, Diethelm A. Surgical treatment of constrictive pericarditis. Ann Surg, 1962; 155: 883-93.
10. Yetkin U, Ilhan G, Calli AO, Yesil M, Gurbuz A. Severe calcific chronic constrictive tuberculous pericarditis. Tex Heart Inst J, 2008; 35: 224-5.
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Sri Lankan Journal of Cardiology Volume 3: Issue 2 – June 2020
Figure 1: Angiography of the right coronary artery
Thereafter, engagement and angiography of the
left coronary artery was performed (Figure 2,
“Spider view” of left coronary artery). However,
there was no culprit lesion noted on the left system.
Figure 2: “Spider view” of left coronary artery
Case Report
A 40-year-old previously healthy male presented
to the District General Hospital, Embilipitiya
following the development of chest pain. The
patient had been admitted within 30 minutes of the
onset of pain. An immediate bed side electro
cardiogram (ECG) revealed changes suggestive of
an inferior STEMI.
The patient was hemodynamically stable with no
features of cardiac failure or cardiac rhythm
disturbances. He was treated with thrombolytic
therapy with standard dosage of intra vascular (IV)
Streptokinase. However, he had poor response to
medical management, remained symptomatic and
was transferred for rescue PCI to the Cardiology
unit, NHSL, Colombo via a hospital ambulance
transfer, a journey that lasted 5 hours.
Upon arrival to the Cardiology unit, NHSL an
echocardiogram performed revealed hypokinesia
of the inferior segments of the heart suggestive of
ongoing ischemia. Thereafter, the patient
underwent coronary angiography to determine the
etiology of ischemia.
Angiography of the right coronary artery (RCA)
did not reveal an obvious culprit lesion (Figure 1).
Ab
stra
ct
Inferior STEMI due to acute occlusion of an
anomalous left circumflex artery arising from
the right coronary cusp and percutaneous
coronary intervention of the anomalous culprit
coronary artery Boralessa MDS1, Sampath Withanawasam 1
1. Institute of cardiology. National Hospital Sri Lanka (NHSL), Colombo
Corresponding Author: Dr. M.D.S. Boralessa
Email: [email protected]
The anomalous origin of the left circumflex artery as an independent branch from the right coronary cusp is a rare variation. These
patients may rarely present with acute coronary syndrome. Therefore, the identification of the culprit lesion and its treatment may
be difficult, particularly in the emergency setting of primary or rescue percutaneous coronary interventions (PCI). We report a case
of a 40-year-old male, who underwent rescue PCI to an anomalous left circumflex artery following failed thrombolysis upon
presentation with an inferior ST elevation myocardial infarction (STEMI) to a rural hospital. This case demonstrates the technical
challenges encountered in making the diagnosis, to enable life saving treatment.
Keywords: Anomalous origin of coronary artery, Anomalous origin of the left circumflex artery, Inferior STEMI, Percutaneous
coronary intervention
.
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Sri Lankan Journal of Cardiology Volume 3: Issue 2 – June 2020
Despite what appeared to be a small caliber left
circumflex artery, there was high suspicion of the
presence of a left circumflex artery with an
anomalous origin due to the following reasons,
1. Presence of ongoing chest pain
2. ECG changes suggestive of Inferior STEMI
3. 2D echo changed suggestive of inferior wall
hypokinesia
4. High titre of Troponin I
Therefore, an angiography of the aortic root was
performed with the use of a pig tail catheter. This
revealed, a large caliber left circumflex artery
with an anomalous origin from the right coronary
cusp as an independent branch. (Figure 3)
Figure 3: large caliber left circumflex artery with an
anomalous origin from the right coronary cusp as an
independent branch
The Left circumflex artery was engaged with a
6F Judkins Right (JR) catheter and upon
angiography was noted to have a near total
occlusion at its mid segment (Figure 4).
Thereafter the patient underwent PCI. A SION
guidewire was used to cross the culprit lesion.
The lesion was pre-dilated with a Mozec 2.0 x
8mm balloon at 4 atm (Figure 5). A Xience Prime
2.75 x 18mm drug eluting stent (DES) was
deployed over the lesion at 10 atm.
Post dilation of the stent was performed with NC
Mozec 2.75 x 8mm balloon at 10 – 14 atm.
Successful reperfusion was achieved with TIMI
III flow and absence of complications (Figure 6).
The patient underwent an uneventful recovery
and was discharged 2 days after PCI. He is at
present receiving follow up care at DGH
Embilipitiya.
Figure 4: Left circumflex artery near total occlusion
at its mid segment
Figure 5: The lesion was pre-dilated with a Mozec
2.0 x 8mm balloon at 4 atm
Figure 6: Successful reperfusion was achieved with
TIMI III flow
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Sri Lankan Journal of Cardiology Volume 3: Issue 2 – June 2020
Discussion
Anomalous origin of the coronary artery is rare.
The clinical importance of this anomaly is
evident from its association as a manifestation of
myocardial ischemia (1).
Anomalous origin of culprit coronary artery
(AOCCA) may either be difficult to diagnose and
can be missed. It can be technically difficult to
perform PCI even in STEMI (2).
Anomalous origin of the left circumflex artery
may be classified according to the site of origin
into different subtypes: left circumflex artery
arising as a direct branch from the right coronary
artery (RCA), a common right system ostium
bifurcating into the left circumflex artery and
RCA, and, as in our case, RCA and left
circumflex artery originating from two separate
orifices (3).
Our patient had classic onset of ischemic type
chest pain along with supportive evidence of
cardiac ischemia by inferior segment ST
elevations on his ECG, elevated troponin I,
echocardiography evidence of inferior wall
hypokinesia and coronary angiography that
revealed near total occlusion of anomalous left
circumflex coronary artery. Despite a delay due
to transfer to reach a PCI facility from a rural
hospital, he underwent PCI that produced
satisfactory results and made a good recovery.
Conclusion This case highlights the need to be vigilant while
evaluating angiography for culprit lesions in the
management of acute coronary syndrome
patients.
It also highlights the need for development of
regional (Provincial/District) cardiac centers
with PCI facilities for management of cardiac
patients and to avoid undue delays in providing
care.
References 1. Samarendra P, Kumari S, Hafeez M, et al.
Anomalous circumflex coronary artery: benign or predisposed to selective atherosclerosis. Angiology, 2001; 52: 521-6
2. Tyczynski P, Kukula T, et al. Anomalous origin of culprit coronary arteries in acute coronary syndromes. Cardio J, 2018; 25(6): 683-690
3. Antopol W, Kugel MA. Anamalous origin of the left circumflex coronary artery. Am Heart J, 1933; 8: 802-6.
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Sri Lankan Journal of Cardiology Volume 3: Issue 2 – June 2020
Heavily calcified coronary arteries carry a formidable challenge in percutaneous coronary interventions. Optimum lesion preparation
plays a key role in both immediate as well as long term clinical outcome in percutaneous coronary interventions in heavily calcified
coronary arteries. Novel devices have markedly improved in their efficacy in delivering excellent results in this aspect. We report a
case of successful Rotablator assisted percutaneous coronary intervention done to a patient who admitted with acute NSTEMI. His
Left ventricular ejection fraction was 50% with inferior wall hypokinesia. His coronary angiogram revealed critical stenosis in mid
RCA which was a heavily calcified vessel. Thus we decided to use the Rotablator to prepare the lesion properly prior to the coronary
intervention. We achieved excellent stent apposition with TIMI 3 flow in distal RCA with resolution of clinical symptoms.
Keywords: Calcific coronary artery, rotational atherectomy,
Subsequently both distal and mid vessel lesions
were successfully stented and post dilatation done
using non-compliant balloon up to 20 ATM. TIMI
3 flow was established in RCA and branches.
Discussion
Percutaneous coronary interventions of heavily
calcified coronary vessels still present an
enormous challenge in interventional cardiology,
with higher risk of immediate complications such
as coronary perforation, late failure due to stent
under expansion and malposition, and
consequently stent restenosis and poor clinical
outcome. Good characterization of calcium
distribution with multimodal imaging is important
to improve the success of treatment. Optimum
lesion preparation is one of the key factors for the
success of such lesions. Therefore, technology has
improved in many ways to develop new tools and
devices. Rotabltor (rotational atherectomy), orbital
atherectomy, laser treatment and coronary
intravascular lithotripsy are promising and
emerging techniques in the field of calcified
coronary arteries. Rotational atherectomy is
relatively cost effective device with a reasonable
learning curve. Most of the time it gives successful
results though it may cause complications such as
coronary artery dissections and burr getting
entrapped. However optimum lesion preparation
in calcified coronary arteries using standard
coronary debulking device will give better short
term as well as long term clinical results.
Delivering coronary devices to the required
stenosed segment becomes easier after using the
rotablator.
Case report
A 62-year-old patient with diabetes mellitus and
dyslipidaemia presented with ischaemic chest pain
to the cardiac ward. She was haemodynamically
stable with clear lung bases. Her ECG revealed ST
depressions in inferior leads with elevated
troponin titer. 2 D echocardiogram revealed
ejection fraction of 50% with inferior wall
hypokinesia. She was treated with loading doses of
dual antiplatelet agents and subcutaneous heparin.
Her chest pain subsided.
Next day, coronary angiography was performed
and it showed heavily calcified right coronary
artery with 99% stenosis at mid vessel and another
90% stenosis at the crux involving proximal PDA.
Left main and left anterior descending arteries
were normal. Left circumflex artery had minor
proximal disease.
Considering the heavily calcified nature of RCA,
rotablator assisted PCI technique was decided.
Right femoral puncture was made and 8 Fr sheath
inserted. Temporary pace maker was kept in situ.
7 Fr Amplatz 1 catheter was used to engage right
coronary ostia. Initially, lesions were crossed with
Sion blue wire and microcathter assisted wire
exchange was done to rotablator floppy wire.
Rotablator functions were checked and several
runs of rotablation done using 1.25mm burr, in mid
vessel and distal lesions. Several cycles were
performed using 1.5mm burr. Slow flow was noted
in distal RCA and corrected with intracoronary
nitrate and adenosine. Both lesions were predilated
with 2.0× 12 mm semi compliant balloon.
Ab
stra
ct
Rotational Atherotomy (Rotablator) assisted
successful PCI in a Heavily Calcified and
Stenosed Right Coronary Artery
Wickramarachchi CP1, Gambhir S2, Lokuketagoda K1, Herath J1,
Amarasena N1
1. Sri Jayewardenepura General Hospital, Sri Lanka.
2. Kailesh University Hospital, India
Corresponding Author: Dr. C P Wickramarachchi E-mail: [email protected]
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Sri Lankan Journal of Cardiology Volume 3: Issue 2 – June 2020
References:
1. Bittl JA, Chew DP, Topol EJ, Kong DF, Califf RM. Metaanalysis of randomized trials of percutaneous transluminal coronary angioplasty versus atherectomy, cutting balloon atherotomy, or laser angioplasty.?J Am Coll Cardiol.?2004;43:936–42. doi: 10.1016/j.jacc.2003.
2. Moreno R, Conde C, Perez-Vizcayno MJ. Prognostic impact of a chronic occlusion in a noninfarct vessel in patients with acute myocardial infarction and multivessel disease undergoing primary percutaneous coronary intervention.?J Invasive Cardiol.?2006;18:16
3. Prasad A, Rihal CS, Lennon RJ, Wiste HJ, Singh M, Holmes DR., Jr. Trends in outcomes after percutaneous coronary intervention for chronic total occlusions: a 25-year experience from the Mayo Clinic.?J Am Coll Cardiol.?2007;49:1611–8. doi: 10.1016/j.jacc.2006.12.040.
4. Ron Waksman SS.?Chronic Total Occlusions: A Guide to Recanalization 2nd edition. In:?John Wiley & Sons, Ltd,?2013:38;2013
5. Fefer P, Knudtson ML, Cheema AN. Current perspectives on coronary chronic total occlusions: the Canadian Multicenter Chronic Total Occlusions Registry. J Am Coll Cardiol. 2012;59:991–7. doi: 10.1016/j.jacc.2011.12.007. [PubMed]
6. King SB, Yeh W, Holubkov R. Balloon angioplasty versus new device intervention: clinical outcomes. A comparison of the NHLBI PTCA and NACI registries. J Am Coll Cardiol. 1998;31:558–66. doi: 10.1016 /S0735-1097(97)10523-X
7. Bittl JA. Directional coronary atherectomy versus balloon angioplasty. N Engl J Med. 1993;329:273–4. doi: 10.1056/NEJM199307223290410. [PubMed]
8. Moliterno DJ. Rotational atherectomy for resistant chronic total occlusions: another spin for tough old problems. Catheter Cardiovasc Interv. 2010;76:372–3. doi: 10.1002/ccd.22752.
9. Walton AS, Pomerantsev EV, Oesterle SN. Outcome of narrowing related side branches after high-speed rotational atherectomy. Am J Cardiol. 1996;77:370–3. doi: 10.1016/S0002-9149(97)89366-6.
10. Tsuchikane E, Suzuki T, Asakura Y. Debulking of chronic coronary total occlusions with rotational or directional atherectomy before stenting: Final results of DOCTORS study. Int J Cardiol. 2008;125:397–403. doi: 10.1016/j.ijcard.2007.07.117.
Figure 1: A stage during procedure
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Sri Lankan Journal of Cardiology Volume 3: Issue 2 – June 2020
Coarctation of aorta (CoA) is a congenital abnormality which can have poor outcome without early intervention. Transcatheter
intervention is the preferable modality of therapy for CoA over surgery. A retrospective analysis of patients’ records was done from
2002-2017, in the Institute of cardiology, National Hospital of Sri Lanka. 50 patients were included with an age range of 8 -50 years
(Mean age was 23.2 years). Male to female ratio was 1.17:1. . Successful outcome was defined by a drop in pressure gradient >50% or
<20mmHg. Majority, 54 %( n=27) had asymptomatic hypertension. All had preserved EF>60% and 50% had LVH on echocardiography.
Bicuspid aortic valves were seen in 22.2%. Mean narrowest diameter of CoA was 4.77mm. The pre-procedural mean PG was
62.93mmHg and post- procedural PG was 11.79mmHg, the reduction was statistically significant (P=0.00). Majority showed
interventional success (93.2%). Procedural failure was seen in 6.3%. Majority, n=39(78%) were free of complications.10 patients (20%)
maintained on long term follow up (84.8 +/-56.9 months). Majority of them had preserved EF. Only 1 patient developed TIA. The study
showed that the transcatheter intervention in CoA shows immediate significant successful results, indicating it as an effective and safe
procedure.
Keywords: Coarctation of aorta (CoA), trans catheter intervention
Material and Methods
A retrospective analysis of patients’ records were
done from 2002-2017, in a tertiary cardiac
specialist centre in Sri Lanka. 50 patients were
included in the analysis.
Results
Number of CoA patients were n=50. Their age
ranged from 8 to 50 years, with a mean age of 23.2
years. Males compromised 54% (n=27) of the
population. Majority, 54% (n=27) had
asymptomatic hypertension. Amongst those
symptomatic, shortness of breath was the
commonest n=10 (43.4%). Headache was seen in
n=4 (17.3%) of symptomatic patients. Most, n=25
(50%) had LVH on 2D echo. All had preserved EF
>60% on initial workup. Eighteen (36%) had co
existing structural abnormalities other than CoA.
Valvular abnormalities were the commonest n=13
(72.2%). Bicuspid aortic valves was seen in n=4
(22.2%), aortic and mitral regurgitation were each
seen in n=3 (16.6%). The narrowest diameter was
1.5mm, and the maximum observed diameter was
15.4mm. Mean was 4.77mm. Eighteen (36%)
underwent only balloon dilation, while n=25
(50%) underwent direct stenting.
Introduction
Coarctation of Aorta (CoA) is a common
congenital cardiac defect resulting in a discrete
narrowing along the lumen of aorta, which can
show anatomical variations (1). The narrowing in
the aortic lumen restricts flow of blood distal to
that of the constriction (2) and results in a process
of maladaptation overtime. Having a
heterogeneous presentation, it can cause increased
mortality by virtue of its impact on the
cardiovascular system. Studies have demonstrated
that when not intervened in a timely manner nearly
75% of patients with CoA die before they reached
50 years (3).
Correction of CoA was initially approached
surgically, but the last four decades have seen
advances in percutaneous intervention to the point
where successful results have been achieved
through endo-vascular intervention, initially
through balloon dilation only, and subsequently
the utilization of stents to place across the
narrowest region. In the Institute of Cardiology,
National Hospital of Sri Lanka transcatheter
intervention for CoA has being done for the last 15
years successfully. In this brief report we attempt
to ascertain the patterns of presentation, clinical,
echocardiographic features, modality of
intervention and immediate outcomes of
coarctation of aorta patients who presented for
transcatheter intervention.
Ab
stra
ct
Clinical and Echocardiographic patterns of
presentation and Immediate outcomes of
Coarctation of aorta patients following
Transcatheter intervention in a Tertiary
Cardiac Intervention centre in Sri Lanka Mendis S A E S 1
1 Institute of Cardiology, National Hospital of Sri Lanka
Corresponding Author: Sepalika Mendis
E-mail: [email protected]
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Sri Lankan Journal of Cardiology Volume 3: Issue 2 – June 2020
Overall procedural intervention was successful,
as the pre-procedural mean PG was 62.93mmHg
and post- procedural PG was 11.79mmHg, the
reduction was statistically significant (P=0.00).
Assessed separately the mean pressure gradient
(PG) before intervention in the balloon dilation
patients was 63.88±33.87mmHg, and 62.24± 21.55
mmHg in the direct stented patients. Post
intervention PG was 20.33±22.5mmHg and 5.64±
9.7mmHg in the balloon dilation and direct
stenting group respectively. However there was no
statistical significance between the mean pressure
gradient difference (42.59mmHg and 54.71mmHg
respectively) following intervention in between left
or right arms (P=0.775). Majority showed
interventional success n=41 (93.2%) [Defined as
a drop in pressure >50% or <20mmHg].
Procedural failure was seen in n=3 (6.3%) of the
analyzed populace, of which n=2 belonged to the
balloon dilation arm. Majority, n=39 (78%) were
free of complications. Four patients had
complications. Aneurysm formation & dissection
were each noted in n=1 (2%) respectively. Only
n=10 (20%) maintained long term follow up. Of
those followed up, the mean duration of follow up
was 84.8 months, with a standard deviation of
56.9months. Most n=9 had preserved ejection
fraction. Most n=9 showed insignificant residual
pressure gradient across CoA. Five remain
symptomatic, n=3 complaining of shortness of
breath and n=2 complaining of chest pain. Most
n=6, had good control of blood pressure. Only 1
patient developed a transient ischemic attack.
Conclusion
Transcatheter intervention of CoA appears to show
immediate significant success, indicating that it as
an effective procedure. Balloon dilation alone or
direct stent insertion has good immediate outcome.
Overall transcatheter management of CoA is a safe
procedure. Complications though uncommon can
be life-threatening. Long term residual persistence
of symptoms and hypertension necessitate the need
for better follow up.
References
1. Torok RD, Campbell MJ, Fleming GA, Hill KD. Coarctation of the aorta: Management from infancy to adulthood. World Journal of Cardiology, 2015; 7(11): 765-75.
2. Vergales JE, Gangemi JJ, Rhueban KS, Lim DS. Coarctation of the Aorta - The Current State of Surgical and Transcatheter Therapies. Current Cardiology Reviews, 2013; 9(3): 211-9.
3. Warnes CA, Williams RG, Bashore TM, Child JS, Connolly HM, Dearani JA, et al. ACC/AHA 2008 Guidelines for the Management of Adults with Congenital Heart Disease: a report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines (writing committee to develop guidelines on the management of adults with congenital heart disease). Circulation., 2008; 118(23): e714-833.
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Sri Lankan Journal of Cardiology Volume 3: Issue 2 - June 2020
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